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    益胃饮对N-甲基-N’-硝基-亚硝基胍诱导的大鼠慢性萎缩性胃炎和胃癌的疗效及机制研究

    Study on the Effect and Mechanism of Yiwei Decoction in the Treatment of N-methyl-N’-nitro-N-nitrosoguanidine-induced Chronic Atrophic Gastritis Rats and Gastric Cancer Rats

      摘要
    • 摘要:
      目的  探究益胃饮对慢性萎缩性胃炎(chronic atrophic gastritis，CAG)和胃癌的治疗作用及其潜在分子机制。
      方法 采用N-甲基-N’-硝基-亚硝基胍(N-methyl-N’-nitro-N-nitrosoguanidine，MNNG)不同周期灌胃分别诱导大鼠CAG和胃癌模型，益胃饮干预后观察其疗效；结合高通量测序和RT-qPCR检测MNNG诱导肿瘤大鼠胃组织及血液中的转录水平差异。
      结果 益胃饮显著改善MNNG诱导的大鼠CAG和肠化生，显著降低MNNG诱导的大鼠胃十二指肠瘤块质量。高通量测序和RT-qPCR验证结果显示，胃组织中Vcan、BGIG10116_32332、rno-miR-542-3p和血清中rno-miR-363-3p的表达在MNNG诱导后显著升高，而益胃饮可以明显逆转这些现象。同时益胃饮可以不同程度地降低VEGFR、HER-2等胃癌治疗靶点的表达水平。
      结论 益胃饮具有治疗MNNG诱导的CAG和肠化生等胃癌前病变的显著疗效，并能进一步抑制MNNG诱导的大鼠胃十二指肠肿瘤进展，其药效机制可能是通过抑制胃部Vcan、lncRNA BGIG10116_32332和rno-miR-542-3p的过表达，及抑制血液中rno-miR-363-3p的过表达。

       

      Abstract:
      OBJECTIVE  To explore the effect and potential molecular mechanisms of Yiwei Decoction on chronic atrophic gastritis(CAG) and gastric cancer.
      METHODS  N-methyl-N’-nitro-N-nitrosoguanidine(MNNG) was used to induce the model of CAG/gastric precancerous lesions and gastric cancer in rats. Therapeutic effect of Yiwei Decoction after intervention was observed. High-throughput sequencing technology and RT-qPCR were used to detect the change of transcriptome in stomach and blood of MNNG-induced tumor rats.
      RESULTS  Yiwei Decoction significantly ameliorated the MNNG-induced CAG and intestinal metaplasia in rats, and significantly reduced the weight of tumor at gastroduodenal junction. Induction of MNNG obviously increased the mRNA level of Vcan, BGIG10116_32332 and rno-miR-542-3p in rat stomach and rno-miR-363-3p in rat serum, while Yiwei Decoction reversed these change. Moreover, Yiwei Decoction could slightly reduce the expression of gastric cancer therapeutic targets including VEGFR and HER-2.
      CONCLUSION  Yiwei Decoction is effective in the treatment of MNNG-induced CAG and intestinal metaplasia; and it can further inhibit the progression of MNNG induced gastric and duodenal tumors in rats. Its pharmacological mechanism may be achieved by inhibiting the overexpression of Vcan, lncRNA BGIG10116-32332, and rno-miR-542-3p in the stomach, as well as suppressing the overexpression of rno-miR-363-3p in the blood.

       

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