Tetrastigma hemsleyanum Diels et Gilg ameliorates lipopolysaccharide induced sepsis via repairing the intestinal mucosal barrier

封堵器 脂多糖 紧密连接 败血症 促炎细胞因子 肿瘤坏死因子α 肠道通透性 肌球蛋白轻链激酶 势垒函数 炎症 细胞凋亡 免疫学 生物 微生物学 细胞生物学 肌球蛋白 生物化学
作者
Lianghui Zhan,Jinbao Pu,Jingru Zheng,Suni Hang,Lisha Pang,Muhua Dai,Chunlian Ji
出处
期刊:Biomedicine & Pharmacotherapy [Elsevier BV]
卷期号:148: 112741-112741 被引量:26
标识
DOI:10.1016/j.biopha.2022.112741
摘要

Sepsis causes excessive systemic inflammation and leads to multiple organ dysfunction syndrome (MODS). The intestine plays a key role in the occurrence and development of sepsis. Tetrastigma hemsleyanum Diels et Gilg (San ye qing, SYQ), a precious Chinese medicine, has been widely used for centuries due to its high traditional value, such as a remarkable anti-inflammatory effect. However, the role of SYQ in intestinal permeability during the development of sepsis needs to be discovered.Mice were intraperitoneally injected with lipopolysaccharide (LPS) to simulate intestinal mucosal barrier function damage in sepsis. Pathological section, inflammatory cytokines, tight junctions, cell apoptosis, and intestinal flora were detected to evaluate the protective effect of SYQ on intestinal mucosal barrier injury in LPS-induced septic mice.The results showed that SYQ treatment obviously attenuated LPS-induced intestinal injury and reduced the production of tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), and interleukin 6 (IL-6). Besides, SYQ also up-regulated the expressions of tight junctions, including Zonula occludens 1 (ZO-1), Claudin-5, and Occludin along with a decreased in the levels of myosin light chain kinase (MLCK) and myosin light chain (MLC). In addition, SYQ down-regulated the expression of Bax/Bcl2 as well as that of cleaved caspase-3 to prevent the cells from undergoing apoptosis. Further, SYQ restored the diversity of the intestinal flora, increased the abundance of Firmicutes, and decreased the abundance of Bacteroidota.The study indicated that SYQ exerted its protective effect on intestinal mucosal barrier injury in LPS-induced septic mice by reducing inflammatory response, improving the tight junction protein expression, inhibiting cell apoptosis, and adjusting the intestinal flora structure.
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