Transretinoic acid inhibits rats gastric epithelial dysplasia induced by N-methyi-N-nitro-N-nitrosoguanidine:influences on cell apoptosis and expression of its regulatory genes

INTRODUCTIONGastric epithelial dysplasia (GED) hypothetically is a straight-forward concept: dysplastic epithelium replacing the normal gastric epithelium of the stomach [1].In the stomach ,like any other segment of the gut ,it is defined as an unequivocal non-invasive epithelial change[2,3].The observation of gastric dysplasia as a cancerous lesion was recognized over a century ago ,but it is only after the advent of gastroscopy that its clinical significance has been stressed[4-7].

EFFECT OF SPLENECTOMY OF GASTRIC CANCER INDUCED WITH N－METHYL－N＇－NITRO－N NITROSOGUANIDINE IN RATS

The wistar rals were given N-methyl-N-nitro-N-nitrosoguanidine (MNNG), 100μg/ml in tap water,to be given ad libitum for 9 months. A total of 80 outbred male wistar rats were equally divided inio 4 groups:Ⅰsplenectomy+MNNG feeding; Ⅱ, omentumectomy + MNNG feeding;Ⅲ, splenectomy only;Ⅳ.omentumectomy only. Among 80 of the rats 23 died within the first 6 months, no cancerous lesion was found (Ⅰ, 0/4, Ⅱ, 0/4, Ⅲ, 0/10, Ⅳ,0/5). Three of the 14 rats that died during the 7th and 8th months were found to present gastric cancer (GC)outgrowth (Ⅰ, 2/4, Ⅱ, 1/5, Ⅲ, 0/3, Ⅳ, 0/2). The rest of the survivors was sacrificed by the end of the 9th month. Thus, the incidence of the GC outgrowth of the various groups were:Ⅰ,14/16 (87.5%); Ⅱ, 10/16 (62.5%), Ⅲ, 0/10;Ⅳ, 0/15.Besides, the cancerous lesions found in groups Ⅰrats appeared to be significantly aggressive than the group Ⅱ rats in terms of depth of invasion and trmor size. In conclusion, the splenectomized rats presented a higher incidence of GC outgrowth,and tended to develop more aggressive tumors.

Direct contact moxibustion promotes apoptosis of gastric cancer cells in rats by regulating intestinal flora

OBJECTIVE:To examine whether direct contact moxibustion(DCM)can prevent and treat gastric cancer(GC)by regulating intestinal flora in rats.METHODS:Male Wistar rats were randomly divided into normal group,normal+DCM control group,model group,and model+DCM group.Gastric cancer rats were induced by N-methyl-N-nitro-N-nitrosoguanidine(MNNG,20 mg/mL)by gavage.At the same time,the model rats and normal rats were given DCM at Zusanli(ST36),Weishu(BL21),and Zhongwan(CV12)for 16 weeks.After treatment,gastric tissues were collected to analyze the pathological changes and the apoptosis of gastric mucosa cells.In addition,the cecal stool was taken and analyzed by 16 s r RNA sequencing.RESULTS:Gastric cancer-like pathological changes and different abundance of the intestinal flora were found in the model group.DCM promoted mucosa tissue apoptosis and regulated the abnormal changes of the intestinal microflora caused by MNNG;DCM also inhibited the growth of Ruminococcaceae and Prevotellaceae flora and promoted the growth of probiotic Akkermansia.Furthermore,DCM made the composition and abundance of intestinal microflora in the GC rats tending to the normal rats.CONCLUSION:DCM stimulating Zusanli(ST36),Weishu(BL21),and Zhongwan(CV12)promoted the apoptosis of gastric mucosa and delayed the progression of gastric cancer,possibly by decreasing Ruminococcaceae and Prevotellaceae bacteria(bacteria that produce short-chain fatty acids in the intestine)and promoting the growth of probiotic Akkermansia.

Protective effect and mechanisms of Weining granule on N-methyl-N’-nitro-N-nitrosoguanidine-induced gastric cancer in rats

OBJECTIVE:To investigate the protective effect and molecular mechanisms of Weining granule on N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced gastric cancer in rats.METHODS:A total of sixty healthy male wistar rats were randomly divided into five groups,including control group (CG),gastric cancer model group (MG),low-dose Weining granule treated group (LWT),medium-dose Weining granule treated group (MWT),and high-dose Weining granule treated group (HWT).Except the control group,the other groups were treated with MNNG to establish a rat model of gastric cancer.Low-dose Weining granule treated group,medium-dose Weining granule treated group,and high-dose Weining granule treated group were fed 9.0,18.0 and 36.0 g/kg Weining granule,respectively.Histopathologic and molecular biologic technology were adopted to determine the protective effect of Weining granule on MNNG-induced gastric cancer in rats.The pathological changes of gastrointestinal tissue were observed.Meanwhile,the differential expression of proliferation,apoptosis and angiogenesis markers were determined,including proliferating cell nuclear antigen (PCNA),pokemon,cyclin D1,B-cell lymphoma-2 (Bcl-2),caspase-3,phosphatase and tensin homolog (PTEN) and vascular endothelial growth factor (VEGF).RESULTS.:After the MNNG treated,the pathological changes of stomach tissue were improved noticeably,including the intestinal metaplasia and atypic hyperplasia.The experiment was completed in.58 rats (96.67%).As compared with gastric cancer model group,the general states of rats were improved significantly after treated with different dose Weining granule.Moreover,treatment with different doses of Weining granule could inhibit the protein and mRNA expression of PCNA,pokemon,cyclin D1,Bcl-2,and VEGF,while increase caspase-3 and PTEN (P < 0.01).CONCLUSION:Weining granule could improve gastric cancer by suppressing cell proliferation,promoting tumor cell apoptosis,and inhibiting angiogenesis.