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作 者:王海娟 李君翔 梁一博 杨平荣 张春江[4] 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;Gansu Medical Products Administration,Lanzhou 730000,China;Gansu Institute for Drug Control,Lanzhou 730000,China;School of Life Sciences,Lanzhou University,Lanzhou 730000,China)
机构地区:[1]甘肃中医药大学药学院,甘肃兰州730000 [2]甘肃省药品监督管理局,甘肃兰州730000 [3]甘肃省药品检验研究院,甘肃兰州730000 [4]兰州大学生命科学学院,甘肃兰州730000
出 处:《中国中药杂志》2024年第18期4996-5005,共10页China Journal of Chinese Materia Medica
基 金:甘肃省科技重大专项(22ZD1FA001);甘肃省科技重大专项企业创新联合体项目(23ZDFA013-3);广州市科技计划项目(2022060106010165);甘肃省重点人才项目(2022RCXM027)。
摘 要:该研究采用植物乳杆菌发酵纹党参,探讨纹党参发酵液(FCR)对急性胃溃疡大鼠胃黏膜的保护作用机制。将64只SD大鼠随机分成8组:空白对照组、模型组、阳性对照组(奥美拉唑)、益生菌组、纹党参未发酵组及FCR低、中、高剂量组,每组8只。采用无水乙醇法对大鼠进行灌胃致急性胃溃疡损伤模型。观察胃黏膜组织的形态学和病理学组织变化,检测各组大鼠胃溃疡面积、抑制率、胃组织抗氧化能力、血清炎症因子及胃黏膜保护因子的表达,测定胃溃疡损伤大鼠肠道菌群的变化情况。结果显示FCR能明显改善胃黏膜组织损伤情况,降低溃疡指数,提高溃疡抑制率,提高大鼠胃组织超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH)、一氧化氮(NO)及胃黏膜保护因子血清前列腺素E2(PGE2)的活性,降低丙二醛(MDA)的含量。与模型组比较,FCR降低了大鼠血清中肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)及髓过氧化物酶(MPO)的活性,此外,无水乙醇损伤大鼠肠道菌群,给予FCR后有效调节了肠道菌群,使得拟杆菌门的相对丰度增加,粪异杆菌属相对丰度减少。即FCR可通过调节抗氧化应激能力、抗炎活性、胃黏膜保护因子的表达及肠道菌群的失衡,从而增强对大鼠急性胃溃疡的保护作用。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.
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