Displaying publications 21 - 40 of 73 in total

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  1. Dh HS, Sultana R, Prabhu A, S R P, Mohanto S, Subramaniyan V
    Biomed Pharmacother, 2024 May;174:116533.
    PMID: 38574626 DOI: 10.1016/j.biopha.2024.116533
    INTRODUCTION: Diabetic nephropathy is a type of kidney disorder that develops as a complication of multifactorial diabetes. Diabetic nephropathy is characterized by microangiopathy, resulting from glucose metabolism, oxidative stress, and changes in renal hemodynamics. This study strived to evaluate the in vitro cytoprotective activity of atorvastatin (ATR), and quercetin (QCT) alone and in combination against diabetic nephropathy.

    METHODS: The MTT assay was utilized to analyze the effects of the test compounds on NRK-52E rat kidney epithelial cells. The detection of apoptosis and ability to scavenge free radicals was assessed via acridine orange-ethidium bromide (AO-EB) dual fluorescence staining, and 2,2-diphenyl-1-picrylhydrazyfree assay (DPPH), respectively. The ability of anti-inflammatory effect of the test compounds and western blot analysis against TGF-β, TNF-α, and IL-6 further assessed to determine the combinatorial efficacy.

    RESULTS: Atorvastatin and quercetin treatment significantly lowered the expression of TGF-β, TNF-α, and IL-6 indicating the protective role in Streptozotocin-induced nephrotoxicity. The kidney cells treated with a combination of atorvastatin and quercetin showed green fluorescing nuclei in the AO-EB staining assay, indicating that the combination treatment restored cell viability. Quercetin, both alone and in combination with atorvastatin, demonstrated strong DPPH free radical scavenging activity and further encountered an anti-oxidant and anti-inflammatory effect on the combination of these drugs.

    CONCLUSION: Nevertheless, there is currently no existing literature that reports on the role of QCT as a combination renoprotective drug with statins in the context of diabetic nephropathy. Hence, these findings suggest that atorvastatin and quercetin may have clinical potential in treating diabetic nephropathy.

    Matched MeSH terms: Kidney/metabolism
  2. Zhang X, Wang J, Xiang S, Zhao L, Lv M, Duan Y, et al.
    Am J Chin Med, 2024;52(6):1795-1817.
    PMID: 39347955 DOI: 10.1142/S0192415X24500708
    Diabetic kidney disease (DKD) has become the primary cause of end-stage renal disease (ESRD), causing an urgent need for preventive strategies for DKD. Astragaloside I (ASI), a bioactive saponin extracted from Astragalus membranaceus (Fisch.) Bunge has been demonstrated to possess a variety of biological activities. This study investigates the therapeutic potential of ASI in DKD and the underlying molecular mechanism using db/db mice in vivo and high glucose (HG)-induced SV40-MES-13 cells in vitro. The results indicated that ASI significantly ameliorated renal dysfunction and mitigated the pathological alterations in the renal tissues of db/db mice. Moreover, ASI was found to reduce the levels of renal fibrosis makers and suppress the activation of TGF-β1/Smad2/3 pathway in both db/db mice and HG-induced SV40-MES-13 cells. Furthermore, ASI downregulated HDAC3 expression, upregulated Klotho expression, and enhanced Klotho release. ASI is directly bound to HDAC3, and the beneficial effects of ASI on Klotho/TGF-β1/Smad2/3-mediciated renal fibrosis in DKD were reversed by the HDAC3 agonist ITSA-1. In conclusion, ASI attenuates renal fibrosis in DKD, and may act through concurrently inhibiting HDAC3 and TGF-β1, thereby regulating HDAC3-mediciated Klotho/TGF-β1/Smad2/3 pathway.
    Matched MeSH terms: Kidney/metabolism
  3. Mailankot M, Jayalekshmi H, Chakrabarti A, Alang N, Vasudevan DM
    Indian J Exp Biol, 2009 Jul;47(7):608-10.
    PMID: 19761047
    Ethanol intoxication resulted in high extent of lipid peroxidation, and reduction in antioxidant defenses (decreased GSH, GSH/GSSG ratio, and catalase, SOD and GPx activities) and (Na+/K+)-ATPase activity in kidney. Alpha-tocopherol treatment effectively protected kidney from ethanol induced oxidative challenge and improved renal (Na+/K+)-ATPase activity. Ethanol induced oxidative stress in the kidney and decreased (Na+/K+)-ATPase activity could be reversed by treatment with ascorbic acid.
    Matched MeSH terms: Kidney/metabolism*
  4. Huang B, Sui WD, Zhang ZT, Zhao L, Li YY, Yang DH, et al.
    J Biochem Mol Toxicol, 2025 Jan;39(1):e70056.
    PMID: 39812124 DOI: 10.1002/jbt.70056
    Phospholipase A2 receptor 1 (PLA2R1) exists in many animals and plays an important role in membranous nephropathy. In this study, we aimed to evaluate a PLA2R1 knock-in rat model with repaired kidney function to study the molecular mechanisms of membranous nephropathy. We constructed the PLA2R1 knockout [PLA2R1(-)] model and PLA2R1 knock in [PLA2R1(+)] model in rats. Consistent complement C3 and IgA expression was confirmed through colocalization studies. Urinary biochemical indicators were performed using Automatic Biochemistry Analyzer. The complement C3, IgG, and Nephrin were detected by immunofluorescence assay. The expression levels of complement C3, IgA, and PLA2R1 were detected by western blot. The differential expression proteins (DEPs) between control and PLA2R1(+) models were detected by liquid chromatography with tandem mass spectrometry. The PLA2R1(-) model showed proteinuria, complement C3 aggregation, and IgA and IgG deposition in the glomerulus. Comparing with the PLA2R1(-) model, the PLA2R1(+) model, the deposition of complement C3 and IgA in the glomerulus did not completely disappear, and IgG expression weakened. Moreover, the absolute value of urinary protein was much lower in the PLA2R1(+) model than in the PLA2R1(-) model, and some of the humanized PLA2R1 gene fragments repaired some of the kidney functions. Humanized PLA2R1-insertion in rats can repair part of the renal function and reduce proteinuria, which will help in studying the molecular mechanisms of membranous nephropathy, as well as the entire membranous nephropathy-related system and complement activation signaling pathway.
    Matched MeSH terms: Kidney/metabolism
  5. Syed RU, Moni SS, Hussein W, Alhaidan TMS, Abumilha SMY, Alnahdi LK, et al.
    Sci Rep, 2025 Feb 05;15(1):4369.
    PMID: 39910087 DOI: 10.1038/s41598-025-87319-7
    Cubebin, a dibenzyl butyrolactone lignan belonging to several distinct families, including Aristolochiaceae, Myristicaceae, Piperaceae, and Rutaceae, and possesses several pharmacological activities, including analgesic, anti-inflammatory, antioxidant, and vasodilatory. The current study aimed to evaluate the effect of cubebin on streptozotocin (STZ)-evoked diabetic nephropathy (DN). DN is a well-identified complication of diabetes mellitus (DM) characterized by renal hypertrophy that progressively declines kidney function. Wistar rats were randomly divided into groups- normal, STZ control (65 mg/kg/body weight), and STZ + cubebin (10 and 20 mg/kg). Biochemical parameters such as glucose levels, kidney parameters, lipid profile, oxidative stress, endogenous antioxidant markers, inflammatory cytokines and histopathology were performed. Molecular docking [(PDB ID: TNF-α (7JRA), NF-κB (1SVC), TGF-β1 (3TZM)] and dynamic simulation (MDS) were also performed with the selected target. STZ-induced DN was changes in these parameters. In contrast, DN + cubebin at 10 and 20 mg/kg doses improved the biochemical parameters and histological changes. Furthermore, molecular docking and simulation studies showed a binding affinity with negative binding energy with TNF-α (7jra, - 11.342 kcal/mol), TGF-β1 (3tzm, - 9.162 kcal/mol) and NF-κB (1svc, - 6.665 kcal/mol). The results of MDS provided insight into the mechanisms that associate proteins TNF-α, NF-κB, and TGF-β1 in conformational dynamics upon binding to cubebin. In conclusion, these findings exhibit a potential effect of cubebin in STZ-evoked DN rats.
    Matched MeSH terms: Kidney/metabolism
  6. Chitra P, Bakthavatsalam B, Palvannan T
    Biomed Pharmacother, 2014 Sep;68(7):881-5.
    PMID: 25194446 DOI: 10.1016/j.biopha.2014.07.017
    Rheumatoid arthritis in HIV patients undergoing HAART is associated with increased risk of side effect. Elevation of uric acid (UA) is important in tissue damage, deposition of crystal in joints leads to the development of rheumatoid arthritis in the HAART complaint group. This study was carried out to investigate the relationship of uric acid, RA factor, ANA, ESR, cystatin C, urea and creatinine in the HAART complaint group. Moreover; the ratio of uric acid/cystatin C, uric acid/urea and uric acid/creatinine were also studied. To analyze the progression of HIV, the immunological parameters were correlated with uric acid. Our result showed a statistically high significant increase in uric acid, RA factor, ANA, ESR, cystatin C, urea and creatinine in the HAART complaint group when compared to HAART non-complaint group, early stage and control. The ratio of uric acid/cystatin C, uric acid/urea, uric acid/creatinine were significantly increased in the HAART complaint group. Statistically significant positive correlation was observed between uric acid and cystatin C, urea, creatinine, absolute CD4 and CD8 count. The increased level of uric acid, RA factor, ANA, ESR, cystatin C and increased ratio of uric acid/cystatin C in the HAART complaint group might conclude the mechanism underlying the increased risk for rheumatoid arthritis in the HAART complaint group which may relate to the combined effects of low-grade inflammation and renal dysfunction.

    Study done in India
    Matched MeSH terms: Kidney/metabolism
  7. Mazhar R, Shazili NA, Harrison FS
    Parasitol Res, 2014 Oct;113(10):3737-43.
    PMID: 25115732 DOI: 10.1007/s00436-014-4039-x
    In February 2013, forty-seven Notched threadfin bream, the Nemipterus peronii, were sampled from the eastern coastal waters of the South China Sea. The concentration of various elements, namely cadmium (Cd), chromium (Cr), copper (Cu), mercury (Hg), strontium (Sr), manganese (Mn), selenium (Se), Lead (Pb), nickel (Ni), aluminum (Al), arsenic (As), iron (Fe), and Zinc (Zn) were analyzed in the liver, muscle, and kidney organs of the host, as well as in their parasites Hysterothalycium reliquens (nematode) and the Paraphilometroides nemipteri (nematode), using inductively coupled plasma mass spectrometry (ICP-MS). The former group of parasites showed highest accumulation capacity for Cr, Cu, Fe, Mn, Se, Ni, and Zn while the latter group had high accumulation potential of As, Hg, Cd, Al, Pb, and Sr. The divergence in heavy-metal accumulation profiles of both nematodes is linked with the specificity of microhabitats, cuticle morphology, and interspecific competition. The outcome of this study indicates that both parasite models can be used for biomonitoring of metal pollution in marine ecosystems.
    Matched MeSH terms: Kidney/metabolism
  8. Koriem KM, Abdelhamid AZ, Younes HF
    Toxicol. Mech. Methods, 2013 Feb;23(2):134-43.
    PMID: 22992185 DOI: 10.3109/15376516.2012.730561
    Caffeic acid (CA) (3,4-dihydroxycinnamic acid) is among the major hydroxycinnamic acids. Hydroxycinnamic acid is the major subgroup of phenolic compounds. Methamphetamine (METH) is a potent addictive psychostimulant. Chronic use and acute METH intoxication can cause substantial medical consequences, including spleen, kidney, liver and heart. The objective of the present study was to evaluate the antioxidant activity of CA to protect against oxidative stress and DNA damage to various organs in METH toxicity. Thirty-two male Sprague Dawley (SD) rats were divided into four equal groups: group 1 was injected (i.p) with saline (1 mL/kg) while groups 2,3 and 4 were injected (i.p) with METH (10 mg/kg) twice a day over five days period. Where 100 & 200 mg/kg of CA were injected (i.p) into groups 3 and 4, respectively one day before exposure to METH injections. Tissue antioxidants and DNA content were evaluated in different tissues. METH decreased glutathione (GSH) and glutathione peroxidase (GPx) levels while increased malondialdehyde (MDA), catalase (CAT) and protein carbonyl levels in brain (hypothalamus), liver, and kidney tissues of rats. METH increased hyperdiploidy in these tissues and DNA damage results. Prior treatment of CA to animals exposed to METH restores the above parameters to the normal levels and preserves the DNA content of these tissues. These results were supported by histopathological investigations. In conclusion, METH induced oxidative stress and DNA damage and pretreatment of CA before METH injections prevented tissue oxidative stress and DNA damage in METH-treated animals.
    Matched MeSH terms: Kidney/metabolism
  9. Murakami M, Adachi N, Saha M, Morita C, Takada H
    Arch Environ Contam Toxicol, 2011 Nov;61(4):631-41.
    PMID: 21424221 DOI: 10.1007/s00244-011-9660-4
    Perfluorinated surfactants (PFSs) in Asian freshwater fish species were analyzed to investigate tissue distribution, temporal trends, extent of pollution, and level of PFS exposure through food intake. Freshwater fish species, namely carp, snakehead, and catfish, were collected in Japan, Vietnam, India, Malaysia, and Thailand, and 10 PFSs, including perfluorooctanesulfonate (PFOS) and perfluorooctanoate, were analyzed by liquid chromatography-tandem mass spectrometry. PFSs in carp in Tokyo were more concentrated in kidneys (Σ10 PFSs = 257 ± 95 ng/g wet weight [ww]) and livers (119 ± 36 ng/g ww) than in ovaries (43 ± 2 ng/g ww) and muscles (24 ± 17 ng/g ww). Concentrations of PFOS and its precursor, perfluorooctane sulfonamide, in livers of carp and in waters in Tokyo showed a dramatic decrease during the last decade, probably because of 3 M's phasing-out of the manufacture of perfluorooctanesulfonyl-fluoride-based products in 2000. In contrast, continuing contamination by long-chain perfluorocarboxylates (PFCAs) with ≥ 9 fluorinated carbons was seen in multiple media, suggesting that these compounds continue to be emitted. PFS concentrations in freshwater fish species in tropical Asian countries were generally lower than those in developed countries, such as Japan, e.g., for PFOS in muscle, Vietnam < 0.05-0.3 ng/g ww; India < 0.05-0.2 ng/g ww; Malaysia < 0.05-0.2 ng/g ww; Thailand < 0.05 ng/g ww; and Japan (Tokyo) = 5.1-22 ng/g ww. Daily intake of short-chain PFCAs with ≤ 8 fluorinated carbons from freshwater fish species in Japan was approximately one order of magnitude lower than that from drinking water, whereas daily intake of PFOS and long-chain PFCAs with ≥ 9 fluorinated carbons from freshwater fish species was comparable with or greater than that from drinking water. Because the risk posed by exposure to these compounds through intake of fish species is a matter of concern, we recommend the continued monitoring of PFS levels in Asian developing countries.
    Matched MeSH terms: Kidney/metabolism
  10. Erejuwa OO, Omotayo EO, Gurtu S, Sulaiman SA, Ab Wahab MS, Sirajudeen KN, et al.
    Int J Vitam Nutr Res, 2010 Jan;80(1):74-82.
    PMID: 20533247 DOI: 10.1024/0300-9831/a000008
    Oxidative stress plays a crucial role in the development of diabetic complications. The aims of this study were to investigate whether honey could reduce hyperglycemia and ameliorate oxidative stress in kidneys of streptozotocin-induced diabetic rats.
    Matched MeSH terms: Kidney/metabolism
  11. Adam Y, Somchit MN, Sulaiman MR, Nasaruddin AA, Zuraini A, Bustamam AA, et al.
    J Ethnopharmacol, 2009 Jul 6;124(1):154-8.
    PMID: 19375494 DOI: 10.1016/j.jep.2009.04.014
    Orthosiphon stamineus has been used in traditional medicine for centuries especially to treat diseases of the urinary system.
    Matched MeSH terms: Kidney/metabolism
  12. Salleh MN, Ismail P, Abdullah AS, Taufiq-Yap YH, Carmichael P
    IUBMB Life, 2004 Jul;56(7):409-16.
    PMID: 15545218
    Studies with clastogenic carcinogen diethylstilbestrol (DES) resulted in a broad of spectrum of toxic and carcinogenic effects in humans and rodents, but the cellular and molecular mechanism(s) by which it induces cancer is not clear. To identify putative genetic targets for p53 in vivo, we applied the cDNA macroarray gene expression profiles associated with apoptosis by comparing p53+/- knockout mice and wild-type mice on the kidney and uterus of female mice. p53+/- knockout mice and wild-type mice were treated with DES (500 micromole kg(-1)) or vehicle i.p once daily for 4 days. Total RNAs were obtained from kidney and uterus of both control and DES-treated. The signal intensities of individual gene spots on the membrane were quantified and normalized to the expression level of the GAPDH gene as an internal control. Our results demonstrated that 16 genes; bad, bax, bcl-2, bcl-w, bcl-x, caspase-3, caspase-7, caspase-8, c-myc, E124, GADD45, mdm2, NKkappab1, p53, p21, Rb and trail were up-regulated and six genes; caspase-1, caspase-2, DR5, E2F1, FasL and iNOS did not changed in response to DES treatment in wild-type mice compared to p53+/- knockout mice. Most genes are involved in cell cycle regulation, signal transduction, apoptosis, or transcription. The greatest changes were seen in bad, bcl-x, mdm2, p53 and p21 gene expression in wild-type mice compared to p53+/- knockout mice. In comparing p53 and p21 gene expression in wild-type mice and p53+/- knockout mice, there was an 4.4-fold vs. 1.8-fold; 8-fold vs. 5.2-fold for kidney and 16-fold vs. 5.5-fold; 2.1-fold vs. 8.3-fold for uterus samples increase in induction (respectively). RT-PCR and densitometric analysis was used to confirm the biggest changes of p21, p53 and bax genes. Using this approach, we have identified apoptosis associated genes regulated in response to DES and have revealed putative differences between the isogenic parent strain and p53+/- knockout mice, which will contribute to a better understanding of toxicity/carcinogenicity mechanisms in this model.
    Matched MeSH terms: Kidney/metabolism
  13. Dharmani M, Mustafa MR, Achike FI, Sim MK
    Regul. Pept., 2005 Jul 15;129(1-3):213-9.
    PMID: 15927718
    The present study investigated the action of des-aspartate-angiotensin I (DAA-I) on the pressor action of angiotensin II in the renal and mesenteric vasculature of WKY, SHR and streptozotocin (STZ)-induced diabetic rats. Angiotensin II-induced a dose-dependent pressor response in the renal vasculature. Compared to the WKY, the pressor response was enhanced in the SHR and reduced in the STZ-induced diabetic rat. DAA-I attenuated the angiotensin II pressor action in renal vasculature of WKY and SHR. The attenuation was observed for DAA-I concentration as low as 10(-18) M and was more prominent in SHR. However, the ability of DAA-I to reduce angiotensin II response was lost in the STZ-induced diabetic kidney. Instead, enhancement of angiotensin II pressor response was seen at the lower doses of the octapeptide. The effect of DAA-I was not inhibited by PD123319, an AT2 receptor antagonist, and indomethacin, a cyclo-oxygenase inhibitor in both WKY and SHR, indicating that its action was not mediated by angiotensin AT2 receptor and prostaglandins. The pressor responses to angiotensin II in mesenteric vascular bed were also dose-dependent but smaller in magnitude compared to the renal vasculature. The responses were significantly smaller in SHR but no significant difference was observed between STZ-induced diabetic and WKY rat. Similarly, PD123319 and indomethacin had no effect on the action of DAA-I. The findings reiterate a regulatory role for DAA-I in vascular bed of the kidney and mesentery. By being active at circulating level, DAA-I subserves a physiological role. This function appears to be present in animals with diseased state of hypertension and diabetes. It is likely that DAA-I functions are modified to accommodate the ongoing vascular remodeling.
    Matched MeSH terms: Kidney/metabolism
  14. Ahmad A, Sattar MA, Azam M, Abdulla MH, Khan SA, Hashmi F, et al.
    PLoS One, 2016;11(5):e0154995.
    PMID: 27191852 DOI: 10.1371/journal.pone.0154995
    The purpose of the present study was to investigate the interaction between H2S and NO (nitric oxide) in the kidney and to evaluate its impact on the functional contribution of α1A and α1B-adrenoreceptors subtypes mediating the renal vasoconstriction in the kidney of rats with left ventricular hypertrophy (LVH). In rats the LVH induction was by isoprenaline administration and caffeine in the drinking water together with intraperitoneal administration of H2S. The responsiveness of α1A and α1B to exogenous noradrenaline, phenylephrine and methoxaminein the absence and presence of 5-methylurapidil (5-MeU) and chloroethylclonidine (CEC) was studied. Cystathione gamma lyase (CSE), cystathione β synthase (CBS), 3-mercaptopyruvate sulphar transferase (3-MST) and endothelial nitric oxide synthase (eNOS) were quantified. There was significant up regulation of CSE and eNOS in the LVH-H2S compared to the LVH group (P<0.05). Baseline renal cortical blood perfusion (RCBP) was increased (P<0.05) in the LVH-H2S compared to the LVH group. The responsiveness of α1A-adrenergic receptors to adrenergic agonists was increased (P<0.05) after administration of low dose 5-Methylurapidil in the LVH-H2S group while α1B-adrenergic receptors responsiveness to adrenergic agonists were increased (P<0.05) by both low and high dose chloroethylclonidine in the LVH-H2S group. Treatment of LVH with H2S resulted in up-regulation of CSE/H2S, CBS, and 3-MST and eNOS/NO/cGMP pathways in the kidney. These up regulation of CSE/H2S, CBS, and 3-MST and eNOS/NO/cGMP pathways enhanced the responsiveness of α1A and α1B-adrenoreceptors subtypes to adrenergic agonists in LVH-H2S. These findings indicate an important role for H2S in modulating deranged signalling in the renal vasculature resulting from LVH development.
    Matched MeSH terms: Kidney/metabolism*
  15. Lau CL, Chan ST, Selvaratanam M, Khoo HW, Lim AY, Modamio P, et al.
    Fundam Clin Pharmacol, 2015 Aug;29(4):404-16.
    PMID: 26011058 DOI: 10.1111/fcp.12126
    Tyrosine kinase inhibitor sunitinib (used in GIST, advanced RCC, and pancreatic neuroendocrine tumors) undergoes CYP3A4 metabolism and is an ABCB1B and ABCG2 efflux transporters substrate. We assessed the pharmacokinetic interaction with ibuprofen (an NSAID used by patients with cancer) in Balb/c male and female mice. Mice (study group) were coadministered (30 min apart) 30 mg/kg of ibuprofen and 60 mg/kg of sunitinib PO and compared with the control groups, which received sunitinib alone (60 mg/kg, PO). Sunitinib concentration in plasma, brain, kidney, and liver was measured by HPLC as scheduled and noncompartmental pharmacokinetic parameters estimated. In female control mice, sunitinib AUC0→∞ decreased in plasma (P < 0.05), was higher in liver and brain (P < 0.001), and lower in kidney (P < 0.001) vs. male control mice. After ibuprofen coadministration, female mice showed lower AUC0→∞ in plasma (P < 0.01), brain, liver, and kidney (all P < 0.001). However, in male mice, AUC0→∞ remained unchanged in plasma, increased in liver and kidney, and decreased in brain (all P < 0.001). The tissue-to-plasma AUC0→∞ ratio was similar between male and female control mice, but changed after ibuprofen coadministration: Male mice showed 1.6-fold higher liver-to-plasma ratio (P < 0.001) while remained unchanged in female mice and in kidney (male and female mice) but decreased 55% in brain (P < 0.05). The tissue-to-plasma partial AUC ratio, the drug tissue targeting index, and the tissue-plasma hysteresis-like plots also showed sex-based ibuprofen-sunitinib drug interaction differences. The results illustrate the relevance of this DDI on sunitinib pharmacokinetics and tissue uptake. These may be due to gender-based P450 and efflux/transporters differences.
    Matched MeSH terms: Kidney/metabolism
  16. Silva MS, Lúcio-Oliveira F, Mecawi AS, Almeida LF, Ruginsk SG, Greenwood MP, et al.
    Physiol Rep, 2017 Mar;5(6).
    PMID: 28336818 DOI: 10.14814/phy2.13210
    Excessive sodium (Na+) intake in modern society has been associated with several chronic disorders such as hypertension. Several studies suggest that early life events can program physiological systems and lead to functional changes in adulthood. Therefore, we investigated behavioral and neuroendocrine responses under basal conditions and after 48 h of water deprivation in adult (60-day-old Wistar rats) male, Wistar rats originating from dams were offered only water or 0.15 mol/L NaCl during pregnancy and lactation. Early life salt exposure induced kidney damage, as shown by a higher number of ED-1 positive cells (macrophages/monocytes), increased daily urinary volume and Na+ excretion, blunted basal water intake and plasma oxytocin levels, and increased plasma corticosterone secretion. When challenged with water deprivation, animals exposed to 0.15 mol/L NaCl during early life showed impaired water intake, reduced salt preference ratio, and vasopressin (AVP) secretion. In summary, our data demonstrate that the perinatal exposure to excessive Na+ intake can induce kidney injury in adult offspring and significantly affect the key mechanisms regulating water balance, fluid intake, and AVP release in response to water deprivation. Collectively, these novel results highlight the impact of perinatal programming on the homeostatic mechanisms regulating fluid and electrolyte balance during exposure to an environmental stress (i.e. dehydration) in later life.
    Matched MeSH terms: Kidney/metabolism
  17. Lee SK, Sirajudeen KN, Sundaram A, Zakaria R, Singh HJ
    J Physiol Biochem, 2011 Jun;67(2):249-57.
    PMID: 21210316 DOI: 10.1007/s13105-010-0070-2
    Although melatonin lowers blood pressure in spontaneously hypertensive rats (SHR), its effect following antenatal and postpartum supplementation on the subsequent development of hypertension in SHR pups remains unknown. To investigate this, SHR dams were given melatonin in drinking water (10 mg/kg body weight/day) from day 1 of pregnancy until day 21 postpartum. After weaning, a group of male pups continued to receive melatonin till the age of 16 weeks (Mel-SHR), while no further melatonin was given to another group of male pups (Maternal-Mel-SHR). Controls received plain drinking water. Systolic blood pressure (SBP) was measured at 4, 6, 8, 12 and 16 weeks of age, after which the kidneys were collected for analysis of antioxidant enzyme profiles. SBP was significantly lower till the age of 8 weeks in Maternal-Mel-SHR and Mel-SHR than that in the controls, after which no significant difference was evident in SBP between the controls and Maternal-Mel-SHR. SBP in Mel-SHR was lower than that in controls and Maternal-Mel-SHR at 12 and 16 weeks of age. Renal glutathione peroxidase (GPx) and glutathione s-transferase (GST) activities, levels of total glutathione and relative GPx-1 protein were significantly higher in Mel-SHR. GPx protein was however significantly higher in Mel-SHR. No significant differences were evident between the three groups in the activities of superoxide dismutase, catalase and glutathione reductase. In conclusion, it appears that while antenatal and postpartum melatonin supplementation decreases the rate of rise in blood pressure in SHR offspring, it however does not alter the tendency of offspring of SHR to develop hypertension.
    Matched MeSH terms: Kidney/metabolism
  18. Hor YY, Ooi CH, Khoo BY, Choi SB, Seeni A, Shamsuddin S, et al.
    J Med Food, 2019 Jan;22(1):1-13.
    PMID: 30592688 DOI: 10.1089/jmf.2018.4229
    Aging is an inevitable and ubiquitous progress that affects all living organisms. A total of 18 strains of lactic acid bacteria (LAB) were evaluated on the activation of adenosine monophosphate-activated protein kinase (AMPK), an intracellular energy sensor mediating lifespan extension. The cell-free supernatant (CFS) of Lactobacillus fermentum DR9 (LF-DR9), Lactobacillus paracasei OFS 0291 (LP-0291), and Lactobacillus helveticus OFS 1515 (LH-1515) showed the highest activation of AMPK and was further evaluated. The phosphorylation of AMPK by these three LAB strains was more evident in U2OS and C2C12 cells, compared to the other cell lines and control (P 
    Matched MeSH terms: Kidney/metabolism
  19. Gautam A, Paudel YN, Abidin S, Bhandari U
    Hum Exp Toxicol, 2019 Mar;38(3):356-370.
    PMID: 30526076 DOI: 10.1177/0960327118817862
    The current study investigated the role of guggulsterone (GS), a farnesoid X receptor antagonist, in the choline metabolism and its trimethylamine (TMA)/flavin monooxygenases/trimethylamine-N-oxide (TMAO) inhibiting potential in a series of in vitro and in vivo studies as determined by high-performance liquid chromatography (HPLC), mass spectroscopy (MS), and liquid chromatography (LC)-MS techniques. Atherosclerosis (AS) was successfully induced in a group of experimental animals fed with 2% choline diet for 6 weeks. Serum lipid profiles such as total cholesterol, triglycerides, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and very low-density lipoprotein cholesterol were measured. Pro-inflammatory cytokines levels, markers for a hepatic injury, and oxidative stress markers were assessed. Interestingly, GS reduced the level of TMA/TMAO in both in vitro and in vivo studies as demonstrated by the peaks obtained from HPLC, MS, and LC-MS. Furthermore, GS exhibited cardioprotective and antihyperlipidemic effects as evidenced by the attenuation of levels of several serum lipid profiles and different atherogenic risk predictor indexes. GS also prevented hepatic injury by successfully restoring the levels of hepatic injury biomarkers to normal. Similarly, GS inhibited the production of pro-inflammatory cytokines levels, as well as GS, enhanced antioxidant capacity, and reduced lipid peroxidation. Histopathological study of aortic sections demonstrated that GS maintained the normal architecture in AS-induced rats. On the basis of results obtained from current investigation, we suggest that GS might have a great therapeutic potential for the treatment of AS.
    Matched MeSH terms: Kidney/metabolism
  20. Eleazu C, Ekeleme CE, Famurewa A, Mohamed M, Akunna G, David E, et al.
    PMID: 30659555 DOI: 10.2174/1871530319666190119101058
    BACKGROUND: Research studies that holistically investigated the effect of administration of Virgin Coconut Oil (VCO) on diabetic humans or animals are limited in literature.

    OBJECTIVE: To investigate the effect of administration of VCO on lipid profile, markers of hepatic and renal dysfunction, and hepatic and renal antioxidant activities of alloxan induced diabetic rats.

    METHODS: Twenty-four male albino rats were used, and they were divided into four groups of six rats each. Group 1 (Normal Control, NC) received distilled water (1 mL/kg); Group 2 (VCO Control) received VCO (5 mL/kg); Group 3 (Diabetic Control, DC) received distilled water (1 mL/kg); Group 4 (Test Group, TG) received 5 ml/kg of VCO.

    RESULTS: There were no significant differences in blood glucose, body weights, relative liver weights, relative kidney weights, hepatic and renal Superoxide Dismutase (SOD) activities, Malondialdehyde (MDA), albumin, aspartate Amino Transaminase (AST), alanine Amino Transaminase (ALT), Alkaline Phosphatase (ALP), urea, creatinine, uric acid, total cholesterol, triacylglycerol, Very Low Density Lipoprotein cholesterol (VLDL) and Low Density Lipoprotein cholesterol (LDL) concentrations; significant increases in renal Glutathione (GSH), hepatic catalase, Glutathione Peroxidase (GPx) and GSH but significant reduction in renal GPx and catalase activities of VCO control group compared with NC group. There were significant increases in blood glucose, relative liver and kidney weights, hepatic GPx, hepatic and renal MDA concentration, ALP, AST, ALT, urea, creatinine, uric acid, triacylglycerol, total cholesterol, LDL and VLDL concentrations; and significant decreases in body weight, hepatic SOD and GSH activities and albumin concentration but no significant difference in hepatic catalase activity of DC group compared with NC group. Administration of VCO to diabetic rats positively modulated these parameters compared with the diabetic control.

    CONCLUSION: The study showed the potentials of VCO in the management of hyperlipidemia, renal and hepatic dysfunctions imposed by hyperglycemia and by oxidative stress in diabetic rats.

    Matched MeSH terms: Kidney/metabolism*
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