Wang Feifei, Yin Jiajing, Ma Yujin, Jiang Hongwei, Li Yanbo
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.
Mol Med Rep. 2017 Mar;15(3):1079-1086. doi: 10.3892/mmr.2017.6114. Epub 2017 Jan 12.
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.
糖尿病（DM）是一种慢性代谢性疾病，其主要发病机制是胰腺β细胞功能障碍或损伤。炎症导致胰腺β细胞功能逐渐衰竭，β细胞数量减少，这可能是由于胰腺β细胞凋亡或死亡所致，这一点已经得到了充分证实。牡荆素是植物中一种主要的生物活性黄酮类化合物，具有多种药理特性，包括抗氧化、抗炎和抗髓过氧化物酶。牡荆素是否能保护胰腺β细胞免受脂多糖（LPS）诱导的促炎细胞因子产生和凋亡的影响，目前鲜受关注。本研究调查了牡荆素对LPS诱导的胰腺β细胞损伤和凋亡的潜在影响。结果显示，经牡荆素处理后，大鼠胰岛组织和INS-1细胞中LPS诱导的凋亡和损伤显著减少。此外，用牡荆素预处理可降低LPS诱导的大鼠体内促炎细胞因子肿瘤坏死因子-α和高迁移率族蛋白B1（HMGB1）的水平。进一步的实验表明，牡荆素预处理可抑制LPS诱导的INS-1细胞中P38丝裂原活化蛋白激酶信号通路的激活。总之，结果表明牡荆素可通过抑制HMGB1释放来预防LPS诱导的大鼠胰岛组织损伤以及INS-1细胞损伤和凋亡。因此，本研究提供了明确的证据表明牡荆素可能是治疗糖尿病的一种可行的治疗策略。
