Wang Kun, Ma Lin, Wang Hua, Tang Chun-Zhi, Huang De-Yu
College of Health Science, Guangdong Pharmaceutical University, Guangzhou 510310, China; Guangdong Engineering Research Center for Light and Health, Guangzhou 510310.
Department of General Internal Medicine, Chenxinghai Hospital, Zhongshan 528415, Guangdong Province.
Zhen Ci Yan Jiu. 2020 May 25;45(5):384-8. doi: 10.13702/j.1000-0607.190189.
To observe the effect of acupoint catgut embedding on histopathological changes of gastric mucosa and expression of mucosal hypoxia inducible factor (HIF)-1α and vascular endothelial growth factor (VEGF) proteins in chronic atrophic gastritis (CAG) rats, so as to explore its mechanisms underlying improvement of CAG.
Male SD rats were divided into blank group (=10) and model group (=9) and catgut embedment group (=10). The CAG model was established by free drinking of N-methyl-N'-nitro-N-nitroso-guanidine solution (100 μg/mL) and irregular diet. Catgut embedment was applied to "Zhongwan" (CV12) and bilateral "Zusanli" (ST36) and "Pishu" (BL20), once every 10 days, 6 times in total. Histopathological changes of gastric mucosal tissue were observed under microscope after H.E. staining. The expression of HIF-1α and VEGF proteins in the antrum of stomach was detected by Western blot.
H.E. staining showed that compared with the blank group, the number of rats with glandular necrosis, atrophy and mucosal stasis in the model group were increased significantly (<0.001, <0.05).Compared with the model group, the number of rats with gland necrosis, atrophy and mucosal stasis in the catgut embedment group were significantly reduced (<0.01, <0.05). Western blot displayed that the expression levels of HIF-1α and VEGF proteins were significantly higher in rats with blood stasis and model group than in those without blood stasis and the blank group (<0.01), and were considerably down-regulated in the catgut embedment group than in the model group (<0.05, <0.01).
Acupoint catgut embedment can improve the injury of gastric mucosa in CAG rats, which may be associated with its function in down-regulating the expression of HIF-1α and VEGF proteins in the gastric mucosa.
观察穴位埋线对慢性萎缩性胃炎(CAG)大鼠胃黏膜组织病理学变化及黏膜缺氧诱导因子(HIF)-1α和血管内皮生长因子(VEGF)蛋白表达的影响,以探讨其改善CAG的作用机制。
将雄性SD大鼠分为空白组(n = 10)、模型组(n = 9)和埋线组(n = 10)。通过自由饮用N-甲基-N'-硝基-N-亚硝基胍溶液(100μg/mL)并给予不规则饮食建立CAG模型。穴位埋线选取“中脘”(CV12)、双侧“足三里”(ST36)和“脾俞”(BL20),每10天埋线1次,共6次。苏木精-伊红(H.E.)染色后在显微镜下观察胃黏膜组织的病理变化。采用蛋白质免疫印迹法检测胃窦组织中HIF-1α和VEGF蛋白的表达。
H.E.染色显示,与空白组相比,模型组出现腺管坏死、萎缩及黏膜瘀血的大鼠数量显著增加(P<0.001,P<0.05)。与模型组相比,埋线组出现腺管坏死、萎缩及黏膜瘀血的大鼠数量显著减少(P<0.01,P<0.05)。蛋白质免疫印迹法显示,血瘀组和模型组大鼠HIF-1α和VEGF蛋白表达水平显著高于非血瘀组和空白组(P<0.01),且埋线组大鼠HIF-1α和VEGF蛋白表达水平较模型组显著下调(P<0.05,P<0.01)。
穴位埋线可改善CAG大鼠胃黏膜损伤,其机制可能与下调胃黏膜组织中HIF-1α和VEGF蛋白表达有关。