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Devesh Mishra Pathology Pdf 336

Diabetic cardiomyopathy (DCM) is considered to be a clinical pathology independent of concomitant vascular diseases and can be primarily caused by disturbances in the energy substrate [269]. In the high-sucrose and HFD/streptozotocin (STZ)-induced rat DCM model, BBR (10, 30 mg/kg/d, p.o., 16wk) significantly prevented diastolic and systolic dysfunction, and cardiac hypertrophy [269]. Phosphatidylcholine (PC), phosphatidylethanolamine (PE) and sphingolipid (SM) are potential biomarkers of DCM, and the protective effect of BBR on DCM can be through reversal of PC, PE and SM metabolic disturbances [269]. BBR treatment (100 mg/kg/d, p.o., 16wk) of diabetic rats can partially improve cardiac function and significantly reduce FSI, FBG, total TC and TG levels. The underlying mechanism can be that BBR activated cardiac AMPK and Akt in diabetic rats and inhibited GSK3β activity [270]. Similarly, in the palmitate-induced H9C2 cell hypertrophy model, BBR up-regulated alpha-myosin heavy chain (α-MHC) expression, down-regulated beta-myosin heavy chain (β-MHC) expression and thus inhibited H9C2 cell hypertrophy [270]. Moreover, BBR also enhanced AMPK and Akt activation in H9C2 cells and inhibited GSK3β activity [270, 271]. Diabetic hearts are more sensitive to I/R injury, and BBR treatment protected the heart of diabetic rats from I/R damage [272]. This protective effect of BBR was achieved by activating AMPK and Akt activity, while inhibiting GSK3β activity in non-ischemic regions of the diabetic rat hearts [272].

Devesh Mishra Pathology Pdf 336


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