Yang Zongbao, Wang Chenguang, Chen Jiaolong, Wang Hong, Wang Yadong, Ma Fuqiang
Zhongguo Zhen Jiu. 2015 Dec;35(12):1269-73.
To explore the molecular mechanism of moxibustion at stomach meridian acupoints for precancerous lesions of chronic atrophic gastritis (CAG).
Fifty male SD rats were randomly divided into a normal group, a model group, a stomach meridian group, a control point group and a vitacoenzyme group, 10 rats in each group. The CAG precancerous lesion model was made in all the groups except the normal group. The rats in the normal group and model group were bundled for 30 min per day; the rats in the stomach meridian group and control point group were bundled and treated with moxibustion at stomach meridian acupoints or control points for 30 min per day; the rats in the vitacoenzyme group were treated with intragastric administration of vitacoenzyme, once per day. All the treatment was given for 20 weeks. The pathological morphological change of gastric mucosa was observed under optical microscope; the expression of epidermal growth factor (EGF), transforming growth factor alpha (TGF-alpha), vascular endothelial growth factor (VEGF), gastric mucosal proliferatig cell nuclear antigen (PCNA), argyrophilic protein of nucleolar organizer regions (Ag-NORs) in gastric mucosal cells were detected by enzyme linked immuno sorbent assay (ELISA).
Compared with the normal group, in the model group the gastric mucosal cells showed dysplasia and the expression of EGF, TGF-alpha, PCNA, VEGF, Ag-NORs in gastric mucosa cells in the model group was increased significantly (all P < 0.05). Compared with the model group, the gastric mucosa lesion gradually recovered and the expression of EGF, TGF-alpha, PCNA, VEGF, Ag-NORs in gastric mucosal cells was gradually decreased in the stomach meridian group, control point group and vitacoenzyme group, in which the stomach meridian group had the most significant effects (all P < 0.05).
Moxibustion at stomach meridian acupoints can obviously decrease the expression of cell proliferative factors in gastric mucosa in rats with CAG precancerous lesions, inhibit the gastric mucosal cell dysplasia, and promote the recovery of gastric mucosa.
探讨艾灸胃经穴位对慢性萎缩性胃炎(CAG)癌前病变的分子机制。
将50只雄性SD大鼠随机分为正常组、模型组、胃经组、对照点组和维酶素组,每组10只。除正常组外,其余各组均制备CAG癌前病变模型。正常组和模型组大鼠每天捆绑30分钟;胃经组和对照点组大鼠捆绑并分别艾灸胃经穴位或对照点30分钟;维酶素组大鼠灌胃维酶素,每天1次。所有处理均持续20周。光镜下观察胃黏膜病理形态变化;采用酶联免疫吸附测定(ELISA)法检测胃黏膜细胞中表皮生长因子(EGF)、转化生长因子α(TGF-α)、血管内皮生长因子(VEGF)、胃黏膜增殖细胞核抗原(PCNA)、核仁组成区嗜银蛋白(Ag-NORs)的表达。
与正常组比较,模型组胃黏膜细胞出现异型增生,模型组胃黏膜细胞中EGF、TGF-α、PCNA、VEGF、Ag-NORs的表达明显增加(均P<0.05)。与模型组比较,胃经组、对照点组和维酶素组胃黏膜病变逐渐恢复,胃黏膜细胞中EGF、TGF-α、PCNA、VEGF、Ag-NORs的表达逐渐降低,其中胃经组作用最显著(均P<0.05)。
艾灸胃经穴位可明显降低CAG癌前病变大鼠胃黏膜细胞增殖因子的表达,抑制胃黏膜细胞异型增生,促进胃黏膜恢复。