Dataset on anti-human insulin-degrading enzyme activities of cyclic tetra peptides: Insight from insilico approach.

In this work, the biochemical activities of seven cyclic peptides were investigated using the insilico approach. The materials used in this work were Spartan 14 for quantum chemical analysis, molecular operating environment software for molecular docking and ADMETSAR 2.0 for pharmacokinetic investigation. The calculated features obtained for each compound were explored and it was observed that the molecules used in this research have potential anti-human insulin-degrading enzyme activities. Also, (3S,6S,9S)-9-((R)-1-(benzyloxy)ethyl)-6-methyl-3-(4-methylphenethyl)-1,4,7,10-tetraazacyclododecane-2,5,8,11-tetraone (compound 2) with highest binding affinity (-7.95349026 kcal/mol) possess utmost ability to inhibit human insulin-degrading enzyme (PDB id: 2g56) than other investigated compounds and acarbose (referenced compound). The pharmacokinetic analysis for compound 2 was examined and compared to the predicted report for the referenced compound.

Evaluation of Testicular Function and Structural Changes of Wistar Rats Following Antiretroviral Exposure: Protective Role of Cyperus Esculentus.

Long-term antiretroviral drug toxicity may exacerbate the impact of HAART-Cyperus esculentus (C. esculentus) interactions on testicular function in HIV-infected individuals. This study examined the ability of C. esculentus plants to treat testicular dysfunction, which is thought to be a probable side effect of antiretroviral toxicity. Adult Wistar male rats weighing 90-110 g were divided into six groups and administered the prescribed treatments. In addition to testicular histology and stereological parameters, testosterone levels, follicle-stimulating hormone levels, antioxidant markers, malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione levels were also evaluated. The adverse consequences of highly active antiretroviral therapy (HAART) include considerable loss of germ cells, enlargement of the tubular lumen, widening of interstitial gaps, and severe hypocellularity. Compared to the other treatment groups, MDA levels dramatically increased, whereas GSH and antioxidant enzyme (SOD) levels significantly decreased. Testicular architecture was largely conserved after treatment with C. esculentus, with a notable increase in the cellular densities of germinal and interstitial cells and a notable decrease in the tubular lumen. Vacuolation, architectural malformations, and hypoplastic changes were reduced. Significant improvements were also observed in C. esculentus in terms of elevated antioxidant SOD and GSH levels and decreased MDA levels. C. esculentus reduced architectural distortions and testicular dysfunction caused by HAART, and improved testicular morphology. Further exploration of these pathways is required.

Restoration of cardiac metabolic flexibility by acetate in high-fat diet-induced obesity is independent of ANP/BNP modulation.

The present study hypothesized that cardiac metabolic inflexibility is dependent on cardiac atrial natriuretic peptide/brain natriuretic peptide (ANP/BNP) alteration and histone deacetylase (HDAC) activity. We further sought to investigate the therapeutic potential of short-chain amino acid (SCFA) acetate in high-fat diet (HFD)-induced obese rat model. Adult male Wistar rats were assigned into groups (n = 6 per group): Control, Obese, and Sodium acetate (NaAc)-treated and Obese + NaAc-treated groups received distilled water once daily (oral gavage), 40% HFD ad libitum, 200 mg/kg NaAc once daily (oral gavage), and 40% HFD + NaAc, respectively. The treatments lasted for 12 weeks. HFD resulted in increased food intake, body weight, and cardiac mass. It also caused insulin resistance and enhanced ß-cell function, increased fasting insulin, lactate, plasma and cardiac triglyceride, total cholesterol, lipid peroxidation, tumor necrosis factor-α, interleukin-6, HDAC, and cardiac troponin T and γ-glutamyl transferase, and decreased plasma and cardiac glutathione with unaltered cardiac ANP and BNP. However, these alterations were averted when treated with acetate. Taken together, these results indicate that obesity induces defective cardiac metabolic flexibility, which is accompanied by an elevated level of HDAC and not ANP/BNP alteration. The results also suggest that acetate ameliorates obesity-induced cardiac metabolic inflexibility by suppression of HDAC and independent of ANP/BNP modulation.