Objective: To investigate the nephroprotective effect of quercetin (QT) against renal injury induced by titanium dioxide nanoparticles (NTiO2) in rats.
Methods: NTiO2-intoxicated rats received 50 mg/kg of NTiO2 for seven days. The QT + NTiO2 group was pretreated with QT for seven days before being administered NTiO2. Uric acid, creatinine, and blood urea nitrogen were considered to be biomarkers of nephrotoxicity. Catalase (CAT) and superoxide dismutase (SOD) activities and renal levels of malondialdehyde (MDA) were measured to assess the oxidative stress caused by NTiO2.
Results: NTiO2 significantly increased the plasma level of the biomarkers. It also significantly decreased the activities of CAT (P = 0.008) and SOD (P = 0.004), and significantly increased the MDA levels (P = 0.007). NTiO2 caused proximal tubule damage, the accumulation of red blood cells, the infiltration of inflammatory cells, and reduced the glomerular diameters, as well as induced apoptosis in the proximal tubules. Pre-treatment with QT attenuated the histological changes, normalised the plasma biomarkers, suppressed oxidative stress, ameliorated the activities of CAT (P = 0.007) and SOD (P = 0.006), and reduced apoptosis (P < 0.001).
Conclusion: QT was found to have a potent protective effect against nephrotoxicity induced by NTiO2 in rats. It also reduced apoptosis caused by NTiO2.
METHODS: Mice were dosed intraperitoneally with mefenamic acid either as a single dose (100 or 200 mg/kg in 10% Dimethyl sulfoxide/Palm oil) or as single daily doses for 14 days (50 or 100 mg/kg in 10% Dimethyl sulfoxide/Palm oil per day). Venous blood samples from mice during the dosing period were taken prior to and 14 days post-dosing from cardiac puncture into heparinized vials. Plasma blood urea nitrogen (BUN) and creatinine activities were measured.
RESULTS: Single dose of mefenamic acid induced mild alteration of kidney histology mainly mild glomerular necrosis and tubular atrophy. Interestingly, chronic doses induced a dose dependent glomerular necrosis, massive degeneration, inflammation and tubular atrophy. Plasma blood urea nitrogen was statistically elevated in mice treated with mefenamic acid for 14 days similar to plasma creatinine.
CONCLUSION: RESULTS from this study suggest that mefenamic acid as with other NSAIDs capable of producing nephrotoxicity. Therefore, the study of the exact mechanism of mefenamic acid induced severe nephrotoxicity can be done in this animal model.
Aim: To evaluate the nephroprotective activity of CAE and its fractions in cisplatin-induced nephrotoxicity and to assess whether they compromise the anticancer efficacy of cisplatin.
Materials and methods: Cisplatin-induced renal damage was induced in Ehrlich Ascites Carcinoma (EAC) bearing mice during mild phase of tumor growth. CAE and its butanol (BF) and aqueous (AF) fractions were administered orally from the 5th day for five days. Nephroprotective potential (serum urea, creatinine, renal histology) and effect of VC on cisplatin anticancer efficacy (tumor volume, viable tumor cells, percentage increase in life span (% ILS)) were calculated.
Result: CAE and its fractions significantly reversed the cisplatin-induced renal damage. CAE and BF treated animals showed regeneration of 50%-75% of proximal tubular cells. Compared to EAC control mice, the % ILS of the cisplatin-treated group was 244% and it was further extended to 379% after CAE administration. The % ILS in the CAE treated group was 1.6 times higher than the cisplatin alone treated group. GC-MS study showed the presence of astaxanthin and betulin.
Conclusion: CAE of VC reverses cisplatin-induced kidney damage as well as regenerates proximal tubular epithelial cells, without compromising the anticancer effect of cisplatin. When CAE was further fractionated, the nephroprotective activity was retained, but the beneficial anticancer effect of cisplatin was compromised.
METHOD: The meta-analysis included all studies that examined the effect of prebiotic, probiotic, and synbiotic supplements on one or more renal function parameters and had a control group. We searched July 1967 through to March 2016 MEDLINE, Scopus, and Google Scholar databases.
RESULTS: Of 437 studies, 13 were eligible for inclusion in the meta-analysis. GFR levels tended to be reduced; whereas creatinine levels increased in the intervention group compared with the placebo group, both in a non-significant manner. The pooled effect on BUN demonstrated a significant decline compared with the placebo group (MD, -1.72 mmol/L; 95% confidence interval [CI], -2.93 to -0.51; P = 0.005). Urea significantly decreased after intervention (-0.46 mmol/L; 95% CI, -0.60 to -0.32; P <0.0001). The UA levels significantly increased in the intervention group compared with the placebo group (12.28 µmol/L; 95% CI, 0.85-23.71; P = 0.035).
CONCLUSION: This study showed a significant increase in UA and a decrease in urea and BUN. The use of prebiotic, probiotic, and synbiotic supplements among those with compromised renal function or those at risk for renal failure should be limited until large-scale, well-designed randomized controlled trials prove the safety and efficacy of these supplements in improving renal function.
Methods: We conducted a single-arm intervention study at the Clinical Lab of Community Medicine, Universiti Sains Malaysia, and included 31 healthy individuals aged between 30 and 60 years old. Wet cupping therapy was performed at five treatment points at the beginning of the study and repeated after three months. Health outcomes at baseline, one, three, and four months were assessed for FBS, renal function parameters (urea, creatinine, and uric acid), systolic blood pressure (SBP), and von Willebrand factor (vWF).
Results: Forty-five percent of participants were female, and the mean age of study participants was 44.9±6.4 years. Wet cupping therapy significantly reduced FBS, serum urea, and serum creatinine at one, three, and four months compared with baseline values. Serum uric acid and SBP showed a significant reduction at one and four months compared with baseline. The vWF (a measure of endothelial function) had a 4.0% reduction at four months compared to baseline, with a mean difference of 5.3 (95% confidence interval (CI): 2.20 = 8.55; p = 0.002).
Conclusions: This study provides preliminary support that repeated wet cupping therapy enhances body health status; thus, it could be an effective complementary medicine in disease prevention.
AIMS: To investigate P. niruri leaves aqueous extract (PN) effects on kidney functions, histopathological changes and levels of oxidative stress, inflammation, fibrosis, apoptosis and proliferation in DM.
METHODS: PN was orally administered to streptozotocin-nicotinamide-induced male diabetic rats for 28 days. At the end of the treatment, fasting blood glucose (FBG) and kidney functions were measured. Kidney somatic index, histopathological changes and levels of RAGE, Nrf2, oxidative stress markers (TBARS, SOD, CAT and GPx), inflammatory markers (NFkβ-p65, Ikk-β, TNF-α, IL-1β and IL-6), apoptosis markers (caspase-3, caspase-9 and Bax), fibrosis markers (TGF-β1, VEGF and FGF-1) and proliferative markers (PCNA and Ki-67) were determined by biochemical assays, qPCR, Western blotting, immunohistochemistry or immunofluorescence.
RESULTS: Administration of PN helps to maintain near normal FBG, creatinine clearance (CCr), blood urea nitrogen (BUN), BUN/Cr ratio, serum electrolytes, uric acid and urine protein levels in DM. Decreased RAGE, TBARS and increased Nrf2, SOD-1, CAT and GPx-1 were observed in PN-treated diabetic rat kidneys. Expression of inflammatory, fibrosis and apoptosis markers in the kidney reduced but expression of proliferative markers increased following PN treatment. Lesser histopathological changes were observed in the kidney of PN-treated diabetic rats.
CONCLUSION: PN helps to preserve near normal kidney function and prevents histopathological changes via ameliorating oxidative stress, inflammation, fibrosis and apoptosis while enhancing proliferation of the kidney in DM.