MOXIBUSTION ALLEVIATES GASTRIC PRECANCEROUS LESIONS IN RATS BY PROMOTING CELL APOPTOSIS AND INHIBITING PROLIFERATION-RELATED ONCOGENES.

Li Peng, Yu-Feng Xie, Chen-Guang Wang, Huan-Gan Wu, Mi Liu, Ya-Dong Wang, Fu-Qiang Ma, Xiao-Rong Chang, Zong-Bao Yang
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引用次数: 5

Abstract

Background: It is well known that gastric mucosa dysplasia and intestinal metaplasia are gastric precancerous lesions (GPL). Moxibustion treatment of Liangmen (ST21) and Zusanli (ST36) alleviated the inflammatory response and dysplasia of gastric mucosa in our previous study. The purpose of this study was to further examine the underlying mechanism of moxibustion treatment of ST21 and ST36 on GPL.

Materials and methods: Sixty SD rats were divided into five groups and rats with GPL were treated with either moxibustion (ST), moxibustion (Sham), or vitacoenzyme. B-cell lymphoma 2 (bcl-2), tumor protein p53 (P53) and cellular Myc (C-MYC), which are related to cell apoptosis, proliferating cell nuclear antigen (PCNA), vascular endothelial growth factor (VEGF), argyrophilic nucleolar organizer region proteins (Ag-NORs), which are associated with cell proliferation, and cell signaling proteins, nuclear factor kappa B (NF-κB), epidermal growth factor receptor (EGFR) and phosphorylated extracellular signal regulated kinase (p-ERK), were measured after moxibustion treatment.

Results: Compared with Control group, gastric mucosa in GPL group showed abnormal mucosal proliferation and pathological mitotic figure, the mRNA expression of bcl-2, P53 and C-MYC increased significantly (P < 0.01), the protein expression of PCNA, VEGF, Ag-NORs and the activity of NF-κβ as well as EGFR/ERK signaling proteins also increased significantly (P < 0.01). Moxibustion treatment decreased gastric mucosal proliferation and pathological mitotic figure, down-regulated the mRNA expression of bcl-2, P53, C-MYC (P < 0.01), decreased the protein expression of PCNA, VEGF, Ag-NORs and the activity of NF-κβ as well as EGFR/ERK signaling proteins significantly (P < 0.01). But moxibustion treatment of Sham didn't show the same effect on GPL.

Conclusion: Moxibustion treatment inhibited cell apoptosis and reduced gastric mucosa dysplasia by inhibiting the expression of bcl-2, P53, C-MYC and decreased the activity of NF-κβ as well as EGFR/ERK signaling proteins.

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艾灸通过促进细胞凋亡和抑制增殖相关癌基因减轻大鼠胃癌前病变。
背景:众所周知,胃粘膜发育不良和肠化生是胃癌前病变(GPL)。艾灸两门(ST21)和足三里(ST36)可以减轻胃黏膜的炎症反应和不典型增生。本研究旨在进一步探讨艾灸治疗ST21和ST36对GPL的作用机制。材料与方法:将60只SD大鼠分为5组,分别用艾灸(ST)、艾灸(Sham)和维活酶治疗GPL大鼠。与细胞凋亡相关的B细胞淋巴瘤2 (bcl-2)、肿瘤蛋白p53 (p53)和细胞Myc (C-MYC)、与细胞增殖相关的增殖细胞核抗原(PCNA)、血管内皮生长因子(VEGF)、亲银核仁组织区蛋白(Ag-NORs)、细胞信号转导蛋白、核因子κB (NF-κB)、表皮生长因子受体(EGFR)和磷酸化的细胞外信号调节激酶(p-ERK)、均在艾灸治疗后进行测量。结果:与对照组比较,GPL组胃粘膜粘膜增生异常,病理有丝分裂图出现异常,bcl-2、P53、C-MYC mRNA表达显著升高(P < 0.01), PCNA、VEGF、Ag-NORs蛋白表达及NF-κβ、EGFR/ERK信号蛋白活性显著升高(P < 0.01)。艾灸可降低大鼠胃粘膜增生及病理有丝分裂图,下调bcl-2、P53、C-MYC mRNA表达(P < 0.01),显著降低PCNA、VEGF、Ag-NORs蛋白表达及NF-κβ、EGFR/ERK信号蛋白活性(P < 0.01)。而针刺治疗对GPL无明显影响。结论:艾灸治疗通过抑制bcl-2、P53、C-MYC的表达,降低NF-κβ及EGFR/ERK信号蛋白活性,抑制细胞凋亡,减轻胃黏膜发育不良。
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