Vitexin alleviates lipopolysaccharide‑induced islet cell injury by inhibiting HMGB1 release

Wang,Feifei; Yin,Jiajing; Ma,Yujin; Jiang,Hongwei; Li,Yanbo

doi:10.3892/mmr.2017.6114

Vitexin alleviates lipopolysaccharide‑induced islet cell injury by inhibiting HMGB1 release

Authors:
- Feifei Wang
- Jiajing Yin
- Yujin Ma
- Hongwei Jiang
- Yanbo Li
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Affiliations: Department of Endocrinology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China, Department of Endocrinology, The First Affiliated Hospital of Henan University of Science and Technology, Luoyang, Henan 471003, P.R. China
Published online on: January 12, 2017 https://doi.org/10.3892/mmr.2017.6114
Pages: 1079-1086
Copyright: © Wang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Diabetes mellitus (DM) is a chronic metabolic disease, where the predominant pathogenesis is pancreatic β‑cells dysfunction or injury. It has been well established that inflammation leads to a gradual exhaustion of pancreatic β‑cell function with decreased β‑cell mass likely resulting from pancreatic β‑cells apoptosis or death. Vitexin, a major bioactive flavonoid compound in plants has numerous pharmacological properties, including antioxidant, anti‑inflammatory and antimyeloperoxidase. Whether vitexin can protect pancreatic β‑cells against lipopolysaccharide (LPS)‑induced pro‑inflammatory cytokine production and apoptosis has received little attention. The present study investigated the potential effects of vitexin on LPS‑induced pancreatic β‑cell injury and apoptosis. It was revealed that apoptosis and damage induced by LPS in islet tissue of rats and INS‑1 cells was significantly decreased in response to vitexin treatment. In addition, pretreatment with vitexin decreased the levels of the pro‑inflammatory cytokines tumor necrosis factor‑α and high mobility group box 1 (HMGB1) in LPS‑induced rats. Further experiments demonstrated that vitexin pretreatment suppressed the activation of P38 mitogen‑activated protein kinase signaling pathways in LPS‑induced INS‑1 cells. In conclusion, the results indicated that vitexin prevented LPS‑induced islet tissue damage in rats, and INS‑1 cells injury and apoptosis by inhibiting HMGB1 release. Therefore, the present study provided clear evidence indicating that vitexin may be a viable therapeutic strategy for the treatment of DM.

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