Feng Pingping, Xu Yanfang, Tong Baoyan, Tong Xiaoqun, Bian Yinyan, Zhao Shufen, Shen Hongbo
Department of Digestion, Lin'an District Hospital of Traditional Chinese Medicine, Hangzhou, Zhejiang 311300, P.R. China.
Department of Hepatobiliary Surgery, Quzhou People's Hospital, Quzhou, Zhejiang 324000, P.R. China.
Exp Ther Med. 2020 Feb;19(2):1203-1212. doi: 10.3892/etm.2019.8324. Epub 2019 Dec 13.
The therapeutic effect of saikosaponin a (SSa) on hyperlipidemic pancreatitis (HP) is not completely understood. The aim of the present study was to investigate the therapeutic effect and the underlying mechanism of SSa using a rat model of HP. Following successful establishment of the HP rat model, different doses of SSa (low dose group, 10 mg/kg or high dose group, 20 mg/kg) were administrated. Histopathological examination, the wet/dry (W/D) ratio and myeloperoxidase (MPO) activity of the pancreatic tissues were assessed. The lipid, amylase (AMY), lipase and proinflammatory cytokine profiles in serum, as well as the expression of peroxisome proliferator-activated receptor (PPAR)-γ and the NF-κB signaling pathway-related proteins in pancreatic tissues were evaluated. The results showed that SSa effectively attenuated pancreatic pathological injury and reduced both the W/D ratio and MPO activity compared to the HP model rats. SSa also improved lipid metabolism by significantly decreasing the serum levels of total cholesterol and triglycerides (P<0.05). Following the administration of SSa, the activity of AMY and lipase, as well as the levels of the proinflammatory cytokines tumor necrosis factor-α, interleukin (IL)-1β and IL-6 were reduced, particularly in the high dosage group (P<0.05). Furthermore, SSa activated PPAR-γ expression and suppressed the NF-κB signaling pathway in pancreatic tissues. The present study suggested that SSa attenuated HP in rats by increasing lipid metabolism and inhibiting the release of proinflammatory cytokines via the NF-κB inflammatory pathway. The results from the present study indicated that SSa might be a promising therapeutic agent for the treatment of HP.
柴胡皂苷a（SSa）对高脂血症性胰腺炎（HP）的治疗作用尚未完全明确。本研究旨在利用HP大鼠模型探讨SSa的治疗作用及其潜在机制。成功建立HP大鼠模型后，给予不同剂量的SSa（低剂量组，10 mg/kg；或高剂量组，20 mg/kg）。评估胰腺组织的组织病理学检查、湿/干（W/D）比值和髓过氧化物酶（MPO）活性。检测血清中的脂质、淀粉酶（AMY）、脂肪酶和促炎细胞因子水平，以及胰腺组织中过氧化物酶体增殖物激活受体（PPAR）-γ的表达和NF-κB信号通路相关蛋白。结果显示，与HP模型大鼠相比，SSa有效减轻了胰腺病理损伤，降低了W/D比值和MPO活性。SSa还通过显著降低血清总胆固醇和甘油三酯水平改善了脂质代谢（P<0.05）。给予SSa后，AMY和脂肪酶的活性以及促炎细胞因子肿瘤坏死因子-α、白细胞介素（IL）-1β和IL-6的水平降低，尤其是高剂量组（P<0.05）。此外，SSa激活了胰腺组织中PPAR-γ的表达并抑制了NF-κB信号通路。本研究表明，SSa通过增加脂质代谢和抑制NF-κB炎症途径促炎细胞因子的释放来减轻大鼠的HP。本研究结果表明，SSa可能是一种有前景的HP治疗药物。
