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The acute and subchronic toxicity, along with the anti-type 2 diabetic effects, of a triterpenoid extract from persimmon leaves (Tri DKL) was evaluated in animals. Acute oral toxicity was assessed in Swiss mice, whereas subchronic toxicity was investigated in Wistar rats given Tri DKL at 125 and 375 mg/kg body weight (BW) daily for 90 days. Type 2 diabetes was induced in Swiss mice via an 8-week high-fat diet, followed by a single intraperitoneal injection of streptozotocin (100 mg/kg BW). Diabetic mice were subsequently treated with Tri DKL at 250 and 750 mg/kg BW/day for 2 weeks. Results showed that Tri DKL, even at the highest dose of 2500 mg/kg, did not produce any signs of acute toxicity in mice. In rats, subchronic administration of 125 and 375 mg/kg BW/day caused no significant alterations in general behaviours, haematological parameters or hepatic/renal function markers. In diabetic mice, Tri DKL significantly reduced blood glucose levels at both doses. It also lowered total cholesterol and hepatic malondialdehyde levels. Notably, at 250 mg/kg BW/day, Tri DKL decreased triglyceride levels while improving liver and pancreatic tissue histology. Overall, Tri DKL exhibited no acute or subchronic toxicity in animals and demonstrated hypoglycemic and lipid-lowering effects in type 2 diabetic mice, suggesting potential therapeutic benefits.
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http://dx.doi.org/10.1111/bcpt.70081 | DOI Listing |
Basic Clin Pharmacol Toxicol
August 2025
Faculty of Pharmacy, Hue University of Medicine and Pharmacy, Hue University, Hue City, Vietnam.
The acute and subchronic toxicity, along with the anti-type 2 diabetic effects, of a triterpenoid extract from persimmon leaves (Tri DKL) was evaluated in animals. Acute oral toxicity was assessed in Swiss mice, whereas subchronic toxicity was investigated in Wistar rats given Tri DKL at 125 and 375 mg/kg body weight (BW) daily for 90 days. Type 2 diabetes was induced in Swiss mice via an 8-week high-fat diet, followed by a single intraperitoneal injection of streptozotocin (100 mg/kg BW).
View Article and Find Full Text PDFSci Transl Med
February 2018
Division of Biochemistry, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, SE 171 77 Stockholm, Sweden.
Cancer cells adapt to their inherently increased oxidative stress through activation of the glutathione (GSH) and thioredoxin (TXN) systems. Inhibition of both of these systems effectively kills cancer cells, but such broad inhibition of antioxidant activity also kills normal cells, which is highly unwanted in a clinical setting. We therefore evaluated targeting of the TXN pathway alone and, more specifically, selective inhibition of the cytosolic selenocysteine-containing enzyme TXN reductase 1 (TXNRD1).
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