Wang Hai-Juan, Li Jun-Xiang, Liang Yi-Bo, Yang Ping-Rong, Zhang Chun-Jiang
College of Pharmacy, Gansu University of Chinese Medicine Lanzhou 730000, China.
School of Life Sciences, Lanzhou University Lanzhou 730000, China.
Zhongguo Zhong Yao Za Zhi. 2024 Sep;49(18):4996-5005. doi: 10.19540/j.cnki.cjcmm.20240516.704.
This study aims to decipher the mechanism of the broth of Codonopsis Radix fermented with Lactobacillus plantarum(FCR) on the gastric mucosa in the rat model of acute gastric ulcer. A total of 64 SD rats were randomized into 8 groups: control, model, positive control(omeprazole), probiotic, unfermented Codonopsis Radix, and low-, medium-and high-dose FCR, with 8 rats in each group. The rat model of acute gastric ulcer was established by gavage with anhydrous ethanol. The morphological and pathological changes of the gastric mucosal tissue were observed, and the gastric ulcer index, inhibition rate, antioxidant capacity of gastric tissue, serum levels of inflammatory cytokines and gastric mucosal protective factors were determined in each group. In addition, the changes of intestinal microbiota in the rat model were measured. The results showed that FCR significantly attenuated the damage of the gastric mucosal tissue, reduced the ulcer area, increased the inhibition rate, elevated the levels of superoxide dismutase(SOD), catalase(CAT), glutathione peroxidase(GSH), nitric oxide(NO), and lowered the level of malondialdehyde(MDA) in rat gastric tissue. Compared with the model group, FCR elevated the level of prostaglandin E2(PGE2) and reduced the levels of tumor necrosis factor-α(TNF-α), interleukin-1β(IL-1β) and myeloperoxidase(MPO) in the serum of rats. In addition, anhydrous ethanol damaged the intestinal microbiota of rats, which was mitigated by the administration of FCR. Specifically, FCR increased the relative abundance of Bacteroidetes and decreased the relative abundance of Allobaculum. In conclusion, FCR can protect rats from acute gastric ulcer by exerting antioxidant and anti-inflammatory activities, up-regulating the expression of gastric mucosal protective factors, and restoring the balance of intestinal microbiota.
本研究旨在阐明植物乳杆菌发酵党参汤（FCR）对大鼠急性胃溃疡模型胃黏膜的作用机制。将64只SD大鼠随机分为8组：对照组、模型组、阳性对照组（奥美拉唑）、益生菌组、未发酵党参组以及低、中、高剂量FCR组，每组8只。通过无水乙醇灌胃建立大鼠急性胃溃疡模型。观察胃黏膜组织的形态和病理变化，测定各组的胃溃疡指数、抑制率、胃组织抗氧化能力、血清炎症细胞因子和胃黏膜保护因子水平。此外，检测大鼠模型肠道微生物群的变化。结果表明，FCR显著减轻胃黏膜组织损伤，减小溃疡面积，提高抑制率，升高大鼠胃组织中超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、谷胱甘肽过氧化物酶（GSH）、一氧化氮（NO）水平，降低丙二醛（MDA）水平。与模型组相比，FCR提高大鼠血清中前列腺素E2（PGE2）水平，降低肿瘤坏死因子-α（TNF-α）、白细胞介素-1β（IL-1β）和髓过氧化物酶（MPO）水平。此外，无水乙醇破坏大鼠肠道微生物群，而FCR给药可减轻这种破坏。具体而言，FCR增加拟杆菌门的相对丰度，降低Allobaculum的相对丰度。总之，FCR可通过发挥抗氧化和抗炎活性、上调胃黏膜保护因子表达以及恢复肠道微生物群平衡来保护大鼠免受急性胃溃疡的侵害。
