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目的 探讨壳聚糖抗幽门螺杆菌(Hp)的作用机制。方法 将Hp与壳聚糖溶液作用2 4和4 8h后,取上清液测天冬氨酸转氨酶(AST)活性和葡萄糖含量,并在透射和扫描电镜下观察Hp的细菌形态和超微结构变化。结果 Hp与壳聚糖溶液作用后上清液中渗漏的AST活性和葡萄糖含量显著高于对照组(P <0 .0 1或P <0 .0 5 ) ;透射电镜见Hp形态多样,以球形体为主,并可见V形、U形和不规则形;Hp胞壁变薄不完整,有的菌体细胞壁部分或全部脱落消失,细菌轮廓模糊,结构不清,且发生不同程度的凹陷变形,甚至穿孔和破碎;胞质内容物稀疏,空隙明显扩大;细菌内部结构消失或分布异常,胞质不均匀或密度下降,出现高电子密度颗粒。扫描电镜见Hp形态多样,以球形体为主,并可见U形和不规则形;细菌表面广泛改变,粘附有可折射物质,外观呈毛刺状。结论 壳聚糖可能通过破坏Hp外膜的结构、功能和通透性,使细菌内容物渗出,细菌破裂;且从破损的细胞外膜进入Hp菌内,与胞质作用,扰乱其代谢这两种机制发挥抗Hp作用。
Objective To investigate the mechanism of chitosan against Helicobacter pylori (Hp). Methods After treated with chitosan for 24 h and 48 h, the activities of aspartate aminotransferase (AST) and glucose in supernatant were determined. The morphological and ultrastructural changes of Hp were observed under transmission and scanning electron microscopy Variety. Results The leakage of AST and glucose in the supernatant after treated with Hp and chitosan solution were significantly higher than those in the control group (P <0.01 or P <0.05). The morphological changes of Hp were observed by transmission electron microscopy Spherical body dominated, and visible V-shaped, U-shaped and irregular shape; Hp cell wall thinning incomplete, some cell wall part of all or disappear, the bacteria outline fuzzy, unclear structure, and the occurrence of varying degrees of depression Deformation and even perforation and broken; sparse cytoplasm content, the gap was significantly expanded; the internal structure of the bacteria disappear or abnormal distribution of cytoplasmic uneven or density decreased, the emergence of high electron density particles. Scanning electron microscopy Hp morphological diversity, mainly spherical, and visible U-shaped and irregular shape; bacterial surface widely changed, adherent refractory material, the appearance of burr-like appearance. Conclusions Chitosan may cause the bacterial contents to exude and the bacteria rupture by destroying the structure, function and permeability of the outer membrane of Hp, and enter the Hp bacterium from the damaged extracellular membrane to interact with the cytoplasm to disrupt its metabolism. Two mechanisms exert anti-Hp effects.