BackgroundChronic kidney disease (CKD), including nephrotic syndrome, is a major cause of cardiovascular morbidity and mortality. The literature indicates that CKD is associated with profound lipid disorders due to the dysregulation of lipoprotein metabolism which progresses kidney disease. The objective of this study is to evaluate the protective effects of curcumin on dyslipidaemia associated with adenine-induced chronic kidney disease in rats.MethodsMale SD rats (n = 29) were divided into 5 groups for 24 days: normal control (n = 5, normal diet), CKD control (n = 6, 0.75% w/w adenine-supplemented diet), CUR 50 (n = 6, 50 mg/kg/day curcumin + 0.75% w/w adenine-supplemented diet), CUR 100 (n = 6, 100 mg/kg/day curcumin + 0.75% w/w adenine-supplemented diet), and CUR 150 (n = 6, 150 mg/kg/day curcumin + 0.75% w/w adenine-supplemented diet). The serum and tissue lipid profile, as well as the kidney function test, were measured using commercial diagnostic kits.ResultsThe marked rise in total cholesterol, low-density lipoprotein (LDL) cholesterol, very low-density lipoprotein (VLDL) cholesterol, triglycerides and free fatty acids in serum, as well as hepatic cholesterol, triglyceride and free fatty acids of CKD control rats were significantly protected by curcumin co-treatment (at the dose of 50, 100 and 150 mg/kg). Furthermore, curcumin significantly increased the serum high-density lipoprotein (HDL) cholesterol compared to the CKD control rats but did not attenuate the CKD-induced weight retardation. Mathematical computational analysis revealed that curcumin significantly reduced indicators for the risk of atherosclerotic lesions (atherogenic index) and coronary atherogenesis (coronary risk index). In addition, curcumin improved kidney function as shown by the reduction in proteinuria and improvement in creatinine clearance.ConclusionThe results provide new scientific evidence for the use of curcumin in CKD-associated dyslipidaemia and substantiates the traditional use of curcumin in preventing kidney damage.

Acorus calamus is a plant commonly used as a traditional herbal medicine and possesses the wide range of pharmacological applications. The present study investigated the diuretic and antiurolithiatic activities of an ethanolic extract of Acorus calamus L. (Family: Araceae) rhizome (EEAC). For diuretic activity, three doses of EEAC (250, 500 and 750 mg/kg) were studied, and measurement of the urinary volume and electrolytes (Na+ and K+) concentration were taken as evaluation parameters. On the other hand, ethylene glycol induced urolithiasis (0.75% v/v in drinking water for 28 days) was used to study the antiurolithiatic effect of EEAC at the oral dose of 750 mg/kg in male Wistar albino rats. CYSTONE (750 mg/kg, p.o.) was used as a standard reference drug in the present study. After completion of the 28-days respective treatments, the level of various urolithiatic promoters in the biological samples (urine, serum and kidney homogenate) and renal function were used as criteria for assessing the antiurolithiatic effect of EEAC. Results indicate that, the EEAC (750 mg/kg, p.o.) produced significant increase in urine volume (p < 0.001) and urinary excretion of Na+ and K+ electrolytes (p < 0.05) in a pattern comparable to that of furosemide. In ethylene glycol induced urolithiatic model, EEAC significantly (p < 0.05) decreased excretion and deposition of various urolithiatic promoters as compared to urolithiatic control in a pattern comparable to that of CYSTONE. The EEAC supplementation also prevents the impairment of renal functions. The antiurolithiatic mechanism is mediated possibly through diuretic and nephroprotective actions of the active compounds of rhizomes.

Abstract(R)‐ α ‐lipoic acid (ALA), an essential cofactor in mitochondrial respiration and a potential antioxidant, possesses a wide array of metabolic benefits including anti‐obesity, glucose lowering, insulin‐sensitizing, and lipid‐lowering effects. In this study, the curative effects of ALA (100 mg/kg) on a spectrum of conditions related to metabolic syndrome and type 2 diabetes (T2D) were investigated in a high‐fat diet (HFD)‐fed and low‐dose streptozotocin (STZ)‐induced rat model of metabolic syndrome and T2D. The marked rise in the levels of glucose, triglycerides, total‐cholesterol, LDL‐cholesterol, and VLDL‐cholesterol in the blood of HFD‐fed and low‐dose STZ‐injected rats were significantly reduced by ALA treatment. Furthermore, ALA treatment significantly increased the serum HDL‐cholesterol levels and tended to inhibit diabetes‐induced weight reduction. Mathematical computational analysis revealed that ALA also significantly improved insulin sensitivity and reduced the risk of atherosclerotic lesions and coronary atherogenesis. This study provides scientific evidence to substantiate the use of ALA to mitigate the glucose and lipid abnormality in metabolic syndrome and T2D.

MicroRNAs (miRNAs) are a novel group of universally present small noncoding endogenous RNAs that regulate gene expression and protein coding by base pairing with the 3’ untranslated region (UTR) of target mRNAs. So they have been associated with several physiological processes and play an important role in the manifestation of diverse diseases. miRNAs expression is associated with the normal and diverse pathophysiological state including cardiac hypertrophy, neurodegenerative diseases, diabetes and its complication, and cancer because individual miRNAs are associated with the regulation of the expression of multiple target genes. Modulating the expression of a single miRNA can influence an entire gene network and thereby modify complex disease phenotypes. From recent studies, it has been confirmed that miRNA has a potential physiological role in various body systems. But in some specialized condition over expression of miRNA within the cytoplasm also leads to some pathological condition in the body. Here, we summarize the roles of miRNAs in various pathological conditions and consider the advantages and potential challenges of miRNA-based therapeutic approaches compared to conventional drug-based therapies.

High-carbohydrate containing diets have become a precursor to glucose-mediated protein glycation which has been linked to an increase in diabetic and cardiovascular complications. The aim of the present study was to evaluate the protective effect of (R)-α-lipoic acid (ALA) against glucose-induced myoglobin glycation and the formation of advanced glycation end products (AGEs) in vitro. Methods: The effect of ALA on myoglobin glycation was determined via the formation of AGEs fluorescence intensity, iron released from the heme moiety of myoglobin and the level of fructosamine. The extent of glycation-induced myoglobin oxidation was measured via the levels of protein carbonyl and thiol. Results: The results showed that the co-incubation of ALA (1, 2 and 4 mM) with myoglobin (1 mg/mL) and glucose (1 M) significantly decreased the levels of fructosamine, which is directly associated with the decrease in the formation of AGEs. Furthermore, ALA significantly reduced the release of free iron from myoglobin which is attributed to the protection of myoglobin from glucose-induced glycation. The results also demonstrated a significant protective effect of ALA on myoglobin from oxidative damage, as seen from the decreased protein carbonyls and increased protein thiols. Conclusion: The anti-glycation properties of ALA suggest that ALA supplementation may be beneficial in the prevention of AGEs-mediated diabetic and cardiovascular complications.