OBJECTIVE:To explore the mechanism by which Qinghua decoction(清化饮)regulates neuroendocrine inflammation in chronic nonbacterial prostatitis(CNP)model rats and provide an experimental basis for clinical treatment.ME...OBJECTIVE:To explore the mechanism by which Qinghua decoction(清化饮)regulates neuroendocrine inflammation in chronic nonbacterial prostatitis(CNP)model rats and provide an experimental basis for clinical treatment.METHODS:The rats were randomly divided into six groups:normal control,model,Qianlie Tongyu capsule,low-dose Qinghua decoction,medium-dose Qinghua decoction,and high-dose Qinghua decoction group with six rats in each group.Rats in each group were sacrificed on the 29th day of treatment,and blood and prostate tissues were collected.Serum levels of tumor necrosis factor-alpha and interleukins 1-beta,6,8,and 10(TNF-αand IL-1β,-6,-8,and-10,respectively)were measured using enzyme-linked immunosorbent assay.The pathological changes in the rat prostate tissue in each group were observed under a light microscope.The expression levels of chromogranin A(CgA),nerve growth factor(NGF),and tyrosine kinase A(TrkA)were detected using reverse transcription quantitative polymerase chain reaction.Western blotting was used to detect protein expression of CgA,NGF,and TrkA.RESULTS:In the model group,the prostate capsule membrane and stroma were significantly dilated with more inflammatory cells infiltrating the stroma and perivessels.TNF-α,IL-1β,-6,and-8,CgA,NGF,and TrkA levels increased,whereas the content of IL-10 decreased,which was statistically significant compared to that in the normal control group(P<0.05).Prostate tissue cells in the high-dose group were neatly arranged with no obvious inflammatory cell infiltration.When compared with the model group,the high-dose Qinghua decoction group showed a significant improvement in these indices(P<0.05).CONCLUSION:Qinghua decoction led to inhibition of pathological changes in the prostate tissue of rats with CNP,regulation of inflammatory cytokine expression,and inhibition in the expression of CgA,NGF,and TrkA.This mechanism may be primarily related to regulation of the CgA/NGF/TrkA signaling pathway mediated by various inflammatory factors.展开更多
OBJECTIVE:To explored the mechanism of Buzhong Yigi decoction(补中益气汤 BZYQD) in inhibiting prostatic cell proliferation effect.METHODS:The compounds of BZYQD consisted with eight herbs were searched in TCMSP databa...OBJECTIVE:To explored the mechanism of Buzhong Yigi decoction(补中益气汤 BZYQD) in inhibiting prostatic cell proliferation effect.METHODS:The compounds of BZYQD consisted with eight herbs were searched in TCMSP databases and the putative targets of BZYQD were collected in Drugbank database.Then,“Benign prostatic hyperplasia”(BPH) was used to find the targets based on the Gene Cards,Online Mendelian Inheritance in Man(OMIM) and Therapeutic Target Database(TTD) databases,and they were further used to collect further collect the intersection targets between BZYQD and BPH by counter-selection.Next,Herb-Compound-Target-Disease network was constructed by Cytoscape software and protein interaction network was built by Search tool for recurring instances of neighbouring genes(STRING) database.Gene Ontology(GO) enrichment and Kyoto Encyclopedia of Genes and Genomes(KEGG) pathway enrichment were analyzed by Database for Annotation,Visualization and Integrated Discovery(DAVID) database to predict the mechanism of the intersection targets.Mitogen activated protein kinase 8(MAPK8),interleukin 6(IL-6) and quercetin were chosen to perform molecular docking.Then 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-Htetrazolium bromide(MTT) assay was to detect the via bility of BPH-1(BPH epithelial cell line) by treated with quercetin at the concentrations of 15,30,60,120 μM for 12,24,48,72 h.The production of IL-6,tumor necrosis factor-α(TNF-α),IL-1β and were m RNA expression detected by enzyme-linked immunosorbent assay kit and quantitative real-time polymerase chain reaction.Western blot was used to detect the expression of phospho-p38 mitogen-activated protein kinase(p-P38) and matrix metalloprotein-9(MMP-9).RESULTS:A total 151 chemical ingredients of 8 herbs and 1756 targets in BZYQD,105 common targets of BZYQD and BPH which mainly involving with MAPK8,IL-6,and so on.GO enrichment analysis got 352 GO entries(P < 0.05) which included 208 entries of biological process,64 entries of cell component and 80 entries of molecular function.KEGG pathway Enrichment analyses got 20 significant pathways which mainly involved with MAPK signaling way.MTT assay indicated quercetin inhibited the viability of BPH-1 cells by time-and dosedependent manner.Quercetin decreased the IL-6,TNF-α and IL-1β production and m RNA expression,and the expression of p-P38 and MMP-9 were also obviously reduced after treated with quercetin.CONCLUSIONS:BZYQD inhibited BPH through suppressing inflammatory response which might involving with regulating the MAPK signaling way.展开更多
目的:探究益肾通癃汤对前列腺癌(PCa)皮下种植瘤模型裸鼠N-钙黏蛋白(N-cadherin)、波形蛋白(Vimentin)表达的影响。方法:用前列腺癌PC-3细胞悬液建立PCa皮下种植瘤模型裸鼠,造模成功后将其随机分为模型组、益肾通癃汤低剂量组、益肾通...目的:探究益肾通癃汤对前列腺癌(PCa)皮下种植瘤模型裸鼠N-钙黏蛋白(N-cadherin)、波形蛋白(Vimentin)表达的影响。方法:用前列腺癌PC-3细胞悬液建立PCa皮下种植瘤模型裸鼠,造模成功后将其随机分为模型组、益肾通癃汤低剂量组、益肾通癃汤中剂量组、益肾通癃汤高剂量组,每组10只。各给药组灌胃给予相应药物,模型组灌胃给予等体积生理盐水,2次/d,连续3周。给药结束后,观察裸鼠一般状态,测量体质量及瘤体大小,称重并计算抑瘤率;运用HE染色观察各组裸鼠种植瘤病理学改变;ELISA法检测各组裸鼠血清中N-cadherin、Vimentin的水平;Western blotting检测各组裸鼠种植瘤组织中N-cadherin、Vimentin蛋白表达情况;PCR检测各组裸鼠种植瘤组织中N-cadherin m RNA、Vimentin m RNA表达情况。结果:与模型组比较,益肾通癃汤低、中、高剂量组裸鼠状态均可,瘤体质量,血清中N-cadherin、Vimentin水平,种植瘤组织中N-cadherin、Vimentin的蛋白及m RNA相对表达量均降低(P<0.05),瘤体细胞少量坏死;与益肾通癃汤低剂量组比较,益肾通癃汤中、高剂量组裸鼠一般状态可,瘤体质量,血清中N-cadherin、Vimentin水平、种植瘤组织中N-cadherin、Vimentin蛋白及mRNA相对表达量均降低(P<0.05),瘤体细胞部分坏死;与益肾通癃汤中剂量组比较,益肾通癃汤高剂量组裸鼠一般状态良好,瘤体质量,血清中N-cadherin水平,种植瘤组织中N-cadherin、Vimentin蛋白相对表达量,种植瘤组织中Vimentin mRNA相对表达量均降低(P<0.05),瘤体细胞坏死多;益肾通癃汤高剂量组裸鼠血清中Vimentin水平、种植瘤组织中N-cadherin mRNA相对表达量与益肾通癃汤中剂量组比较,差异无统计学意义(P>0.05);益肾通癃汤低、中、高剂量组裸鼠抑瘤率分别为26.67%、42.45%、66.26%。结论:益肾通癃汤对人前列腺癌PC-3细胞皮下种植瘤模型裸鼠N-cadherin、Vimentin蛋白的表达具有一定的抑制作用,其机制可能与抑制肿瘤上皮间质转化(EMT)过程相关。展开更多
基金Hebei Administration of Traditional Chinese Medicine Project:Study on the Neuroendocrine Mechanism of Chronic Prostatitis Rats Regulated by the Method of Clearing heat and Dampness,Activating Blood and Removing Stasis(No.2019087)Hebei Provincial Department of Education for Postgraduate Innovation Ability Training Project:the Mechanism of Improving Pulmonary Function of COPD Rats with Lung Qi Deficiency by Regulating Intestinal Bacteria with Peitu Shengjin Formula(No.CXZZBS2020151)Provincial Universities Basic Research Funds Special Project:Study on the Mechanism of Shenling Baizhu Powder Based on Lung Intestine Axis to Interfere with the Deficiency of Lung and Spleen in Experimental COPD(YJZ2019010)。
文摘OBJECTIVE:To explore the mechanism by which Qinghua decoction(清化饮)regulates neuroendocrine inflammation in chronic nonbacterial prostatitis(CNP)model rats and provide an experimental basis for clinical treatment.METHODS:The rats were randomly divided into six groups:normal control,model,Qianlie Tongyu capsule,low-dose Qinghua decoction,medium-dose Qinghua decoction,and high-dose Qinghua decoction group with six rats in each group.Rats in each group were sacrificed on the 29th day of treatment,and blood and prostate tissues were collected.Serum levels of tumor necrosis factor-alpha and interleukins 1-beta,6,8,and 10(TNF-αand IL-1β,-6,-8,and-10,respectively)were measured using enzyme-linked immunosorbent assay.The pathological changes in the rat prostate tissue in each group were observed under a light microscope.The expression levels of chromogranin A(CgA),nerve growth factor(NGF),and tyrosine kinase A(TrkA)were detected using reverse transcription quantitative polymerase chain reaction.Western blotting was used to detect protein expression of CgA,NGF,and TrkA.RESULTS:In the model group,the prostate capsule membrane and stroma were significantly dilated with more inflammatory cells infiltrating the stroma and perivessels.TNF-α,IL-1β,-6,and-8,CgA,NGF,and TrkA levels increased,whereas the content of IL-10 decreased,which was statistically significant compared to that in the normal control group(P<0.05).Prostate tissue cells in the high-dose group were neatly arranged with no obvious inflammatory cell infiltration.When compared with the model group,the high-dose Qinghua decoction group showed a significant improvement in these indices(P<0.05).CONCLUSION:Qinghua decoction led to inhibition of pathological changes in the prostate tissue of rats with CNP,regulation of inflammatory cytokine expression,and inhibition in the expression of CgA,NGF,and TrkA.This mechanism may be primarily related to regulation of the CgA/NGF/TrkA signaling pathway mediated by various inflammatory factors.
文摘OBJECTIVE:To explored the mechanism of Buzhong Yigi decoction(补中益气汤 BZYQD) in inhibiting prostatic cell proliferation effect.METHODS:The compounds of BZYQD consisted with eight herbs were searched in TCMSP databases and the putative targets of BZYQD were collected in Drugbank database.Then,“Benign prostatic hyperplasia”(BPH) was used to find the targets based on the Gene Cards,Online Mendelian Inheritance in Man(OMIM) and Therapeutic Target Database(TTD) databases,and they were further used to collect further collect the intersection targets between BZYQD and BPH by counter-selection.Next,Herb-Compound-Target-Disease network was constructed by Cytoscape software and protein interaction network was built by Search tool for recurring instances of neighbouring genes(STRING) database.Gene Ontology(GO) enrichment and Kyoto Encyclopedia of Genes and Genomes(KEGG) pathway enrichment were analyzed by Database for Annotation,Visualization and Integrated Discovery(DAVID) database to predict the mechanism of the intersection targets.Mitogen activated protein kinase 8(MAPK8),interleukin 6(IL-6) and quercetin were chosen to perform molecular docking.Then 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-Htetrazolium bromide(MTT) assay was to detect the via bility of BPH-1(BPH epithelial cell line) by treated with quercetin at the concentrations of 15,30,60,120 μM for 12,24,48,72 h.The production of IL-6,tumor necrosis factor-α(TNF-α),IL-1β and were m RNA expression detected by enzyme-linked immunosorbent assay kit and quantitative real-time polymerase chain reaction.Western blot was used to detect the expression of phospho-p38 mitogen-activated protein kinase(p-P38) and matrix metalloprotein-9(MMP-9).RESULTS:A total 151 chemical ingredients of 8 herbs and 1756 targets in BZYQD,105 common targets of BZYQD and BPH which mainly involving with MAPK8,IL-6,and so on.GO enrichment analysis got 352 GO entries(P < 0.05) which included 208 entries of biological process,64 entries of cell component and 80 entries of molecular function.KEGG pathway Enrichment analyses got 20 significant pathways which mainly involved with MAPK signaling way.MTT assay indicated quercetin inhibited the viability of BPH-1 cells by time-and dosedependent manner.Quercetin decreased the IL-6,TNF-α and IL-1β production and m RNA expression,and the expression of p-P38 and MMP-9 were also obviously reduced after treated with quercetin.CONCLUSIONS:BZYQD inhibited BPH through suppressing inflammatory response which might involving with regulating the MAPK signaling way.
文摘目的:探究益肾通癃汤对前列腺癌(PCa)皮下种植瘤模型裸鼠N-钙黏蛋白(N-cadherin)、波形蛋白(Vimentin)表达的影响。方法:用前列腺癌PC-3细胞悬液建立PCa皮下种植瘤模型裸鼠,造模成功后将其随机分为模型组、益肾通癃汤低剂量组、益肾通癃汤中剂量组、益肾通癃汤高剂量组,每组10只。各给药组灌胃给予相应药物,模型组灌胃给予等体积生理盐水,2次/d,连续3周。给药结束后,观察裸鼠一般状态,测量体质量及瘤体大小,称重并计算抑瘤率;运用HE染色观察各组裸鼠种植瘤病理学改变;ELISA法检测各组裸鼠血清中N-cadherin、Vimentin的水平;Western blotting检测各组裸鼠种植瘤组织中N-cadherin、Vimentin蛋白表达情况;PCR检测各组裸鼠种植瘤组织中N-cadherin m RNA、Vimentin m RNA表达情况。结果:与模型组比较,益肾通癃汤低、中、高剂量组裸鼠状态均可,瘤体质量,血清中N-cadherin、Vimentin水平,种植瘤组织中N-cadherin、Vimentin的蛋白及m RNA相对表达量均降低(P<0.05),瘤体细胞少量坏死;与益肾通癃汤低剂量组比较,益肾通癃汤中、高剂量组裸鼠一般状态可,瘤体质量,血清中N-cadherin、Vimentin水平、种植瘤组织中N-cadherin、Vimentin蛋白及mRNA相对表达量均降低(P<0.05),瘤体细胞部分坏死;与益肾通癃汤中剂量组比较,益肾通癃汤高剂量组裸鼠一般状态良好,瘤体质量,血清中N-cadherin水平,种植瘤组织中N-cadherin、Vimentin蛋白相对表达量,种植瘤组织中Vimentin mRNA相对表达量均降低(P<0.05),瘤体细胞坏死多;益肾通癃汤高剂量组裸鼠血清中Vimentin水平、种植瘤组织中N-cadherin mRNA相对表达量与益肾通癃汤中剂量组比较,差异无统计学意义(P>0.05);益肾通癃汤低、中、高剂量组裸鼠抑瘤率分别为26.67%、42.45%、66.26%。结论:益肾通癃汤对人前列腺癌PC-3细胞皮下种植瘤模型裸鼠N-cadherin、Vimentin蛋白的表达具有一定的抑制作用,其机制可能与抑制肿瘤上皮间质转化(EMT)过程相关。
