Objective:To investigate the therapeutic effect of Sanhuang Xiexin Decoction(SXD)on triplenegative breast cancer(TNBC)in mice and its underlying mechanism.Methods:The high-performance liquid chromatography(HHLC)was us...Objective:To investigate the therapeutic effect of Sanhuang Xiexin Decoction(SXD)on triplenegative breast cancer(TNBC)in mice and its underlying mechanism.Methods:The high-performance liquid chromatography(HHLC)was used to quantitate and qualify SXD.A total of 15 female BALB/c mice were inoculated subcutaneously on the right hypogastrium with 3×10^(5) of 4T1-Luc cells to establish TNBC mouse model.All mice were divided randomly into 3 groups,including phosphate buffered solution(PBS),SXD and doxorubicin(DOX)groups(positive drug).Additionally,tumor growth,pathological changes,serum lipid profiles,expression of Janus kinase 2(JAK2)-signal transducer and activator of transcription 3(STAT3)signaling pathway and its key targets including inflammatory factors,cell cycle and epithelial-mesenchymal transition(EMT)markers were investigated.Besides,the biosafety of SXD was also evaluated in mice.Results:Rhein,coptisine,berberine hydrochloride and baicalin were all found in SXD,and the concentrations of these 4 components were 0.57,2.61,2.93,and 46.04 mg/g3respectively.The mouse experiment showed that SXD could notably suppress the development of tumors and reduce the density of tumor cells(P<0.01).The serum lipid analysis and Oil-Red-O staining both showed the differences,SXD group exhibited higher serum adiponectin and HDL-C levels with lower TC and LDL-C levels compared to the PBS and DOX groups(P<0.05 or P<0.01),respectively.SXD also decreased the levels of phospho-JAK2(p-JAK2),phospho-STAT3(p-STAT3)expressions and its downstream factors,including mostly inflammatory cytokine,EMT markers,S phase of tumor cells and vascular endothelial growth factor(VEGF)expression(P<.05 or P<0.01),respectively.The biosafety assessment of SXD revealed low levels of toxicity in mice.Conclusion:SXD could inhibit TNBC by suppressing JAK2-STAT3 phosphorylation which may be associated with modulation of lipid metabolism.展开更多
OBJECTIVE:To study the effect of methotrexate(MTX) combined with Sanhuang Yilong decoction(SYD) on aquaporin(AQP) expression,and to explore the role of AQPs in the pathogenesis of rheumatoid arthritis(RA).METHODS:A to...OBJECTIVE:To study the effect of methotrexate(MTX) combined with Sanhuang Yilong decoction(SYD) on aquaporin(AQP) expression,and to explore the role of AQPs in the pathogenesis of rheumatoid arthritis(RA).METHODS:A total of 118 dampness-heat blockage type RA patients who were hospitalized in the General Chengdu Military Hospital between January2014 and December 2016 were selected as subjects in this study(30 patient of these patients with knee joint effusion were assigned to the RA synovial fluid group).For the pre-treatment controlgroups,30 healthy volunteers were recruited as the healthy control group and 30 osteoarthritis(OA) patients with knee joint effusion were included as OA synovial fluid control group.The RA dampnessheat blockage syndrome treatment groups were divided into 45 cases in the combined group and 45 cases in the MTX group.The combined group received MTX combined with SYD treatment while the MTX group received MTX alone.AQP1,AQP2 and AQP3 expressions were detected in the serum and synovial fluid.RESULTS:AQP1 had the highest expression,followed by AQP3,and AQP2.The serum levels of AQP1,AQP2 and AQP3 were all significantly lower than those in the healthy volunteers(P < 0.05),while the synovial fluid AQP1,AQP2 and AQP3 expression in the RA group were comparable to these in the OA groups(P > 0.05).After treatment for2 weeks,serum AQP1,AQP2,AQP3 were significantly increased and erythrocyte sedimentation rate,C-reactive protein,disease activity score of 28 joints were decreased in the combined group(P < 0.05).CONCLUSION:Abnormal expression of AQPs inhibits water metabolism in RA dampness-heat blockage syndrome,so liquid is accumulated at the joint,which may play an important role in the pathogenesis of RA.MTX combined with SYD for the treatment of RA can effectively increase AQP expression.展开更多
基金Supported by Natural Science Foundation of Zhejiang Province(No.LY20C060002)。
文摘Objective:To investigate the therapeutic effect of Sanhuang Xiexin Decoction(SXD)on triplenegative breast cancer(TNBC)in mice and its underlying mechanism.Methods:The high-performance liquid chromatography(HHLC)was used to quantitate and qualify SXD.A total of 15 female BALB/c mice were inoculated subcutaneously on the right hypogastrium with 3×10^(5) of 4T1-Luc cells to establish TNBC mouse model.All mice were divided randomly into 3 groups,including phosphate buffered solution(PBS),SXD and doxorubicin(DOX)groups(positive drug).Additionally,tumor growth,pathological changes,serum lipid profiles,expression of Janus kinase 2(JAK2)-signal transducer and activator of transcription 3(STAT3)signaling pathway and its key targets including inflammatory factors,cell cycle and epithelial-mesenchymal transition(EMT)markers were investigated.Besides,the biosafety of SXD was also evaluated in mice.Results:Rhein,coptisine,berberine hydrochloride and baicalin were all found in SXD,and the concentrations of these 4 components were 0.57,2.61,2.93,and 46.04 mg/g3respectively.The mouse experiment showed that SXD could notably suppress the development of tumors and reduce the density of tumor cells(P<0.01).The serum lipid analysis and Oil-Red-O staining both showed the differences,SXD group exhibited higher serum adiponectin and HDL-C levels with lower TC and LDL-C levels compared to the PBS and DOX groups(P<0.05 or P<0.01),respectively.SXD also decreased the levels of phospho-JAK2(p-JAK2),phospho-STAT3(p-STAT3)expressions and its downstream factors,including mostly inflammatory cytokine,EMT markers,S phase of tumor cells and vascular endothelial growth factor(VEGF)expression(P<.05 or P<0.01),respectively.The biosafety assessment of SXD revealed low levels of toxicity in mice.Conclusion:SXD could inhibit TNBC by suppressing JAK2-STAT3 phosphorylation which may be associated with modulation of lipid metabolism.
基金the Army Medical Research Twelfth Five Year Plan Key Project(No.BWS11J06)the Sichuan Provincial Health Department(No.120573)
文摘OBJECTIVE:To study the effect of methotrexate(MTX) combined with Sanhuang Yilong decoction(SYD) on aquaporin(AQP) expression,and to explore the role of AQPs in the pathogenesis of rheumatoid arthritis(RA).METHODS:A total of 118 dampness-heat blockage type RA patients who were hospitalized in the General Chengdu Military Hospital between January2014 and December 2016 were selected as subjects in this study(30 patient of these patients with knee joint effusion were assigned to the RA synovial fluid group).For the pre-treatment controlgroups,30 healthy volunteers were recruited as the healthy control group and 30 osteoarthritis(OA) patients with knee joint effusion were included as OA synovial fluid control group.The RA dampnessheat blockage syndrome treatment groups were divided into 45 cases in the combined group and 45 cases in the MTX group.The combined group received MTX combined with SYD treatment while the MTX group received MTX alone.AQP1,AQP2 and AQP3 expressions were detected in the serum and synovial fluid.RESULTS:AQP1 had the highest expression,followed by AQP3,and AQP2.The serum levels of AQP1,AQP2 and AQP3 were all significantly lower than those in the healthy volunteers(P < 0.05),while the synovial fluid AQP1,AQP2 and AQP3 expression in the RA group were comparable to these in the OA groups(P > 0.05).After treatment for2 weeks,serum AQP1,AQP2,AQP3 were significantly increased and erythrocyte sedimentation rate,C-reactive protein,disease activity score of 28 joints were decreased in the combined group(P < 0.05).CONCLUSION:Abnormal expression of AQPs inhibits water metabolism in RA dampness-heat blockage syndrome,so liquid is accumulated at the joint,which may play an important role in the pathogenesis of RA.MTX combined with SYD for the treatment of RA can effectively increase AQP expression.
