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...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.展开更多
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 co...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.展开更多
基金Supported by the National Nature Science Foundation of China(No.81660743)the Project of Guangxi Scholars+1 种基金the Special Project of Guangxi Traditional Chinese Medicine Administration Bureau(No.GZYZ-10-18)the Project of Guangxi Young Teacher Fundamental Ability Promotion(No.2017KY0298)
文摘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.
基金Supported by the National Natural Science Fund:the Biophysical Properties Research of Related Acupoints Based on the Physiological State of Uterus(No.81603542)Study on Advantages of Disease and the Law of Micro-Needle Therapy by Using Data Mining Technology(No.81473773)+1 种基金the Project of Improving Scientific Research Ability of Hebei University of Chinese Medicine:the Immune Initiation Effect of Dendritic Cells on Rat with Gastric Cancer Treating by Direct Moxibustion(No.KTZ2019012)Postgraduate Innovation Project of Hebei University of Chinese Medicine:the Immune Initiation Effect of Dendritic Cells on Rat with Gastric Cancer Treating by Direct Moxibustion(No.XCXZZBS2020012)。
文摘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.