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Hispolon reduces mitochondrial dysfunction and improves fibrosis of diabetes nephropathy by activating AMPK signal and inhibiting mPTP opening
Hispolon may improve kidney scarring and cell energy problems in diabetic kidney disease by activating energy control and preventing harmful pore opening
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Abstract
Hispolon improved several parameters related to kidney damage in db/db mice and enhanced cell viability in high glucose-induced kidney cells.
- Diabetic nephropathy progression is associated with glomerular damage, collagen deposition, and elevated serum creatinine and urea nitrogen in db/db mice.
- Hispolon intervention reduced renal oxidative stress markers and improved antioxidant enzyme activity.
- The treatment suppressed inflammation and downregulated fibrosis markers in the kidneys.
- Hispolon restored protein levels of p-AMPK, SIRT1, and PGC-1α, which are involved in cellular energy regulation.
- In vitro, Hispolon decreased cell death and oxidative stress in kidney cells exposed to high glucose.
- Mechanistic studies suggest that the AMPK/SIRT1/PGC-1α pathway is crucial for Hispolon's effect on mitochondrial function.
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