Haematuria and Outcomes in Patients with Diabetic Chronic Kidney Disease
Hong Kong Journal of Nephrology
Results: HFHS diet led to vacuolization and thyroidisation of the renal tubules. Glucose caused mitochondrial fragmentation and cellular apoptosis in HK2 cells. Autophagy was activated in glucose-treated cells as evidenced by the enhanced LC3B-II expression and autophagosome formation. When autophagy was inhibited, either by the inhibitor, 3-MA, or by siATG5, tubular cells were more susceptible to glucose-induced mitochondrial fragmentation and cellular apoptosis. When MFN1 or MFN2 was
... r MFN2 was knockdown, mitochondria became more fragmented and autophagy was activated. When FIS1 was silenced, mitochondria were not fragmented and the expressions of LC3B-II, p62 and BECN1 remained unchanged. Conclusion: Our results characterized the pathology of diabetic tubulopathy and suggested that glucose leads to mitochondrial fragmentation and cellular apoptosis in renal tubules. We also offered evidence that autophagy protects mitochondrial from fragmentation in renal tubules. http://dx. Objective: Tangshen Formula (TSF), a traditional Chinese medicine, had been reported to have beneficial effects on diabetic nephropathy (DN), but its action mechanism is still unclear. The study was designed to elucidate the potential mechanism of TSF in treating DN. Methods: Type 2 DN rat models were established by high-fat diet-fed and low-dose-streptozotocin injection. The rats were treated with or without TSF by gavage for 20 weeks and examined by 24h-albuminuria, histology, immunohistochemistry, molecular analyses. Results: The results showed that TSF treatment significantly inhibited urinary excretion of albumin, and attenuated renal histological injuries in the rats. TSF treatment also inhibited renal inflammation which was associated with inactivation of NF-kB signaling. In addition, TSF treatment also suppressed expressions of fibronectin, collagen I, and collagen IV. Conclusion: The present study revealed that TSF might attenuate renal inflammation of type 2 DN by inhibiting NF-kB signaling pathway.