ArticleFrontiers in pharmacology2026
Cepharanthine improves blood glucose levels and mitigates renal injury in streptozotocin-induced diabetic rats via restoring pancreatic β-cell integrity and reducing inflammation.
Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background/Objectives: We have previously demonstrated that the natural alkaloid Cepharanthine (Ceph) reduces renal injury in streptozotocin (STZ)-induced insulin-deficient diabetic rats via antioxidant and anti-inflammatory mechanisms. However, the hypoglycemic mechanism of Ceph remains unclear. We hypothesize that Ceph reduces blood glucose in STZ-induced insulin-deficient diabetic rats via restoring pancreatic β-cells function and insulin secretion. Methods: Diabetes was induced in male Sprague-Dawley rats by a single intraperitoneal injection of STZ (50 mg/kg, i. p). Rats with blood glucose ≥250 mg/dL were confirmed to be diabetic. Rats were randomly assigned to four groups (n = 6/group): Control, Control + Ceph, Diabetic, and Diabetic + Ceph. Rats were treated with either vehicle or Ceph (10 mg/kg/day, i. p) for 6 weeks. Pancreatic β-cell integrity was evaluated using TUNEL assay and pancreatic duodenal homeobox 1 (PDX-1) immunofluorescence. Aortic rings vascular reactivity was assessed using wire myography, and renal function was determined by measuring creatinine clearance, albuminuria, and podocalyxin excretion. Renal inflammation and fibrosis were quantified via ELISA assessment of ICAM-1 and TGF-β and Masson's trichrome staining. Results: Ceph treatment significantly reduced blood glucose levels and increased plasma insulin levels in diabetic rats. The % TUNEL Conclusion: These data suggest that Ceph halts the progression of diabetic nephropathy in rats not only via its antioxidant and anti-inflammatory properties but also via the reduction in pancreatic β-cells apoptosis and increased β-cells integrity in STZ-induced insulin-deficient diabetic male Sprague-Dawley rats.
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