Abstract Title:

Hesperidin ameliorates pancreaticβ-cell dysfunction and apoptosis in streptozotocin-induced diabetic rat model.

Abstract Source:

Life Sci. 2019 Oct 15 ;235:116858. Epub 2019 Sep 7. PMID: 31505195

Abstract Author(s):

Wanthanee Hanchang, Aree Khamchan, Navinee Wongmanee, Chananchida Seedadee

Article Affiliation:

Wanthanee Hanchang


AIMS: The current study was conducted to investigate the potential protective effects of hesperidin and its possible mechanisms of action on pancreaticβ-cells in diabetes.

MAIN METHODS: Male Sprague Dawley rats were made diabetic using 65 mg/kg intraperitoneal injection of streptozotocin, and then administered daily with 100 mg/kg of hesperidin over 4 weeks. On conclusion of the experiment, blood and pancreatic tissue were collected to determine the function of β-cells, apoptosis, oxidative stress, ER stress, and inflammation.

KEY FINDINGS: Treatment of diabetic rats with hesperidin, significantly decreased fasting blood glucose and food intake, along with increased body weight, serum and pancreatic insulin levels, and pancreatic-duodenal homeobox-1 (PDX-1) protein expression. The beneficial roles of hesperidin on diabetic pancreaticβ-cells exhibited an increment in antioxidant SOD and GPx activities, and a decrement in nitrotyrosine as well as malondialdehyde (MDA) levels. Additionally, the elevated concentration of TNF-α and expressions of ER stress maker GRP78 and CHOP proteins in the pancreas of diabetic rats were significantly diminished by hesperidin treatment. Furthermore, hesperidin effectively modulated expressions of apoptosis-regulatory proteins in diabetic rat pancreas, as revealed by upregulating anti-apoptotic Bcl-xL; with a concomitant downregulating pro-apoptotic Bax, cleaved caspase-3, and inhibiting the activation of DNA repair protein poly (ADP-ribose) polymerase (PARP).

SIGNIFICANCE: Collectively, these findings suggest that hesperidin may have the potential to protect pancreaticβ-cells and improve their function by suppressing oxidative and ER stress, along with activating its antioxidant, anti-inflammatory, and anti-apoptotic effects.

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Sayer Ji
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