METHODS: Diabetes was induced using streptozotocin (60 mg/kg, i.v.) followed by nicotinamide (210 mg/kg, intraperitoneal (i.p.)). MAD (50 mg/kg) was administered orally for 4 weeks, commencing 15 days after induction of diabetes; resveratrol (10 mg/kg) was used as a positive control. Fasting blood glucose, plasma insulin, HbA1c, liver and lipid parameters were measured, along with antioxidant enzymes and malondialdehyde as an index of lipid peroxidation; histological and immunohistochemical studies were also undertaken.
KEY FINDINGS: MAD normalized the elevated fasting blood glucose levels. This was associated with increased plasma insulin concentrations. MAD alleviated oxidative stress by improving enzymatic antioxidants and reducing lipid peroxidation. Histopathological examination showed significant recovery of islet structural degeneration and an increased area of islets. Immunohistochemical staining showed increased insulin content in islets of MAD-treated rats.
CONCLUSIONS: The results demonstrate an antidiabetic effect of MAD associated with preservation of β-cell structure and function.
OBJECTIVE: The BP ethanol and methanol extracts were evaluated to determine antioxidant activity by an in vitro method and lyophilized extract of BP was added to beef patties to study oxidative stability.
MATERIALS AND METHODS: Antioxidant activities of extracts of BP were determined by measuring scavenging radical activity against methoxy radical generated by Fenton reaction 2,2'-azino-bis-3-ethylbenzothiazoline-6-sulphonic acid (TEAC) radical cation, the oxygen radical absorbance capacity (ORAC) and the ferric reducing antioxidant power (FRAP) assays. The lipid deterioration in beef patties containing 0.1% and 0.3% (w/w) of lyophilized extract of BP stored in 80:20 (v/v) O2:CO2 modified atmosphere (MAP) at 4 °C for 10 days was determined using thiobarbituric acid reacting substances (TBARS), % metmyoglobin and colour value.
RESULTS: The BP methanol extract revealed the presence of catechin, myricetin, quercetin, naringenin, and p-coumaric acid. The BP ethanol (50% w/w) extract showed scavenging activity in TEAC, ORAC and FRAP assays with values of 1.45, 2.81, 1.52 mmol Trolox equivalents (TE)/g DW, respectively. Reductions in lipid oxidation were found in samples treated with lyophilized BP extract (0.1% and 0.3% w/w) as manifested by the changes of colour and metmyoglobin concentration. A preliminary study film with BP showed retard degradation of lipid in muscle food.
CONCLUSION: The present results indicated that the BP extracts can be used as natural food antioxidants.
PURPOSE: To explore the underlying mechanism of AP in exerting anti-fatigue effects.
METHODS: In this study, we developed a chronic sleep deprivation-induced fatigue model and used physiological, hematological, and biochemical indicators to evaluate the anti- fatigue efficacy of AP. Additionally, a multi-omics approach was employed to reveal the anti-fatigue mechanisms of AP from the perspective of microbiome, metabolome, and proteome.
RESULTS: The detection of physiology, hematology and biochemistry index indicated that AP markedly alleviate mice fatigue state induced by sleep deprivation. The 16S rRNA sequencing showed the AP promoted the abundance of probiotics (Odoribacter, Dubosiella, Marvinbryantia, and Eubacterium) and suppressed harmful bacteria (Ruminococcus). On the other hand, AP was found to regulate the expression of colonic proteins, such as increases of adenosine triphosphate (ATP) synthesis and mitochondrial function related proteins, including ATP5A1, ATP5O, ATP5L, ATP5H, NDUFA, NDUFB, NDUFS, and NDUFV. Serum metabolomic analysis revealed AP upregulated the levels of anti-fatigue amino acids, such as taurine, leucine, arginine, glutamine, lysine, and l-proline. Hepatic proteins express levels, especially tricarboxylic acid (TCA) cycle (CS, SDHB, MDH2, and DLST) and redox-related proteins (SOD1, SOD2, GPX4, and PRDX3), were significantly recovered by AP administration. Spearman correlation analysis uncovered the strong correlation between microbiome, metabolome and proteome, suggesting the anti-fatigue effects of AP is attribute to the energy homeostasis and redox balance through gut-liver axis.
CONCLUSION: AP increased colonic ATP production and improve mitochondrial function by regulating gut microbiota, and further upregulated anti-fatigue amino acid levels in the blood. Based on the gut-liver axis, AP upregulated the hepatic tricarboxylic acid cycle and oxidoreductase-related protein expression, regulating energy homeostasis and redox balance, and ultimately exerting anti-fatigue effects. This study provides insights into the anti-fatigue mechanisms of AP, highlighting its potential as a therapeutic agent.
MATERIALS AND METHODS: Red tea and clove-mediated ZnO NPs were synthesized using the green synthesis method. The anti-microbial activity was tested against oral pathogens using the agar well diffusion method, while the anti-diabetic activity was estimated using the alpha-amylase inhibitory assay method by using red tea and clovemediated ZnO NPs.
RESULTS: ZnO NPs were successfully synthesized using red tea and clove-formulated extract. The synthesized ZnO NPs using Aspalathus linearis (red tea) and Syzygium aromaticum (clove) mediated ZnO NPs were characterized using UV visible spectrophotometry and SEM (Scanning Electron Microscope) analysis. The green synthesized ZnO NPs show promising anti-microbial activity by exhibiting a 12 mm zone of inhibition against S. aureus, 11 mm in E. faecalis, 9 mm in S. mutans, and 11 mm in C. albicans. In anti-diabetic activity, the green synthesized ZnO NPs showed a maximum inhibition percentage of up to 80% at the maximum concentration of 50 µg/mL.
CONCLUSION: Green synthesized ZnO NPs using red tea and clove showed maximum efficacy in anti-microbial properties which can lead to huge potential use as antibacterial agents. Simultaneously, anti-diabetic activity showed an excellent inhibition percentage which can be a potent therapeutic agent in the field of nanomedicine in diabetes management.