A systematic review on nephron protective AYUSH drugs as constituents of NEERI-KFT (A traditional Indian polyherbal formulation) for the management of chronic kidney disease

Chronic Kidney Disease (CKD) is a major health problem characterized by kidney dysfunction with progressive segmental glomerulosclerosis to end-stage renal disease (ESRD). Due to lack of scientific data and comprehensive reports, the current systematic review provides an inclusive understanding and prospective associated with phytopharmacology of NEERI-KFT in CKD. The data was collected from more than five databases such as Science Direct, Google Scholar, Elsevier, PubMed, Springer, ACS publication etc using keywords like CKD/Kidney disease, epidemiology/prevalence, modern therapies for CKD management, NEERI-KFT and its role in kidney disease. The study was performed based on scientific reports screened by experts according to inclusion and exclusion criteria. The pre-clinical and clinical findings suggested that NEERI-KFT has promising effects as nephroprotective and considered safe and well effective in primary care of kidney against disease. Phytopharmacological evaluation of NEERI-KFT suggest that it exhibit substantial potential against oxidative and inflammatory stress induced apoptosis by exerting antioxidants, nephroprotective and immunomodulatory effects. Hence, it can be enlighten that NEERI-KFT have potential herbs which exerts significant antioxidants, nephroprotective and immunomodulatory effects in the patients associated with renal dysfunction or CKD thus improving altered renal architecture and renal physiology. Clinically, it is concluded that NEERI-KFT works kidney malfunction and cease ESRD progression or even reduce the number of dialysis.     

Effect of Cassia auriculata Linn. Root extract on cisplatin and gentamicin-induced renal injury

The ethanol extract of the roots of Cassia auriculata was studied for its nephroprotective activity in cisplatin- and gentamicin-induced renal injury in male albino rats. In the cisplatin model, the extract at doses of 300 and 600 mg/kg body wt. reduced elevated blood urea and serum creatinine and normalized the histopathological changes in the curative regimen. In the gentamicin model, the ethanol extract at a dose of 600 mg/kg body wt. reduced blood urea and serum creatinine effectively in both the curative and the preventive regimen. The extract had a marked nitric oxide free-radical-scavenging effect. The findings suggest that the probable mechanism of nephroprotection by C. auriculata against cisplatin- and gentamicin-induced renal injury could be due to its antioxidant and free-radical-scavenging property.     

Mangiferin attenuates oxidative stress induced renal cell damage through activation of PI3K induced Akt and Nrf-2 mediated signaling pathways

BackgroundMangiferin is a polyphenolic xanthonoid with remarkable antioxidant activity. Oxidative stress plays the key role in tert-butyl hydroperoxide (tBHP) induced renal cell damage. In this scenario, we consider mangiferin, as a safe agent in tBHP induced renal cell death and rationalize its action systematically, in normal human kidney epithelial cells (NKE).MethodsNKE cells were exposed to 20 µM mangiferin for 2 h followed by 50 µM tBHP for 18 h. The effect on endogenous ROS production, antioxidant status (antioxidant enzymes and thiols), mitochondrial membrane potential, apoptotic signaling molecules, PI3K mediated signaling cascades and cell cycle progression were examined using various biochemical assays, FACS and immunoblot analyses.ResultstBHP exposure damaged the NKE cells and decreased its viability. It also elevated the intracellular ROS and other oxidative stress-related biomarkers within the cells. However, mangiferin dose dependently, exhibited significant protection against this oxidative cellular damage. Mangiferin inhibited tBHP induced activation of different pro-apoptotic signals and thus protected the renal cells against mitochondrial permeabilization. Further, mangiferin enhanced the expression of cell proliferative signaling cascade molecules, Cyclin d1, NFκB and antioxidant molecules HO-1, SOD2, by PI3K/Akt dependent pathway. However, the inhibitor of PI3K abolished mangiferin's protective activity.ConclusionsResults show Mangiferin maintains the intracellular anti-oxidant status, induces the expression of PI3K and its downstream molecules and shields NKE cells against the tBHP induced cytotoxicity.General significanceMangiferin can be indicated as a therapeutic agent in oxidative stress-mediated renal toxicity. This protective action of mangiferin primarily attributes to its potent antioxidant and antiapoptotic nature.