Acute lung injury(ALI)is a prevalent and severe clinical condition characterized by inflammatory damage to the lung endothelial and epithelial barriers,resulting in high incidence and mortality rates.Currently,there i...Acute lung injury(ALI)is a prevalent and severe clinical condition characterized by inflammatory damage to the lung endothelial and epithelial barriers,resulting in high incidence and mortality rates.Currently,there is a lack of safe and effective drugs for the treatment of ALI.In a previous clinical study,we observed that Jinyinqingre oral liquid(JYQR),a Traditional Chinese Medicine formulation prepared by the Taihe Hospital,Affiliated Hospital of Hubei University of Medicine,exhibited notable efficacy in treating inflammation-related hepatitis and cholecystitis in clinical settings.However,the potential role of JYQR in ALI/acute respiratory distress syndrome(ARDS)and its anti-inflammatory mechanism remains unexplored.Thus,the present study aimed to investigate the therapeutic effects and underlying molecular mechanisms of JYQR in ALI using a mouse model of lipopolysaccharide(LPS)-induced ALI and an in vitro RAW264.7 cell model.JYQR yielded substantial improvements in LPS-induced histological alterations in lung tissues.Additionally,JYQR administration led to a noteworthy reduction in total protein levels within the BALF,a decrease in MPAP,and attenuation of pleural thickness.These findings collectively highlight the remarkable efficacy of JYQR in mitigating the deleterious effects of LPS-induced ALI.Mechanistic investigations revealed that JYQR pretreatment significantly inhibited NF-κB activation and downregulated the expressions of the downstream proteins,namely NLRP3 and GSDMD,as well as proinflammatory cytokine levels in mice and RAW2647 cells.Consequently,JYQR alleviated LPS-induced ALI by inhibiting the NF-κB/NLRP3/GSDMD pathway.JYQR exerts a protective effect against LPS-induced ALI in mice,and its mechanism of action involves the downregulation of the NF-κB/NLRP3/GSDMD inflammatory pathway.展开更多
Objective: To investigate the protective effectof Qidongyixin Oral Liquidon cultured rat cardiomyocytes infected withCVB 3 . Methods:Monolayer culture of spontaneously contracting rat heart cells were obtained from ne...Objective: To investigate the protective effectof Qidongyixin Oral Liquidon cultured rat cardiomyocytes infected withCVB 3 . Methods:Monolayer culture of spontaneously contracting rat heart cells were obtained from new born SD rats and seeded into culture plates. Results:Chronic Pulmonary Emphysema was lightened,Qidongyixin Oral Liquidcould inhibit the release of cardiac cytosolic enzymes-lactic acid dehydrogenase and glutamic-pyruvic transaminase. Conclusion: Qidongyixin Oral Liquidhas protective effects on viral myocarditis.展开更多
Objective:The effect of prevention and treatment of Xinkang oral liquid(心康口服液,XKOL)on experimental coxsackievirus B_(3)(CVB_(3))myocarditis mice model were investigated.Methods:The mice were inoculated intraperit...Objective:The effect of prevention and treatment of Xinkang oral liquid(心康口服液,XKOL)on experimental coxsackievirus B_(3)(CVB_(3))myocarditis mice model were investigated.Methods:The mice were inoculated intraperitoneally with 0.3 ml of 105 TCID 50 of CVB_(3)to induce acute viral myocarditis model.These mice were divided into model control group(Group A),prevention high dosage group(Group B)and prevention low dosage group(Group C),treatment high dosage group(Group D)and treatment low dosage group(Group E),respectively.In addition,XKOL control group(Group F)and normal control group(Group G)were not infected with CVB_(3)intraperitoneally.The administration of XKOL in Group B and C began 2 days before virus infection.All animals were sacrificed on day 20 for evaluation.Results:Histological examination showed extensive myocardial necrosis and cell infiltration in most of Group A mice,but necrosis and cell infiltration were less severe in Group B,C,D and E mice.Thymus weight in Group B,C,D and E mice were heavier and less cell depletion occurred than those in Group A.Conclussion:The XKOL could effectively inhibit myocardial CVB_(3)replication,reduce the myocardial inflammatory response,lower incidence rate of myocarditis and prevent the disease associated lymphoid organ atrophy in this animal models.展开更多
目的:通过研究金欣口服液含药血清对呼吸道合胞病毒(RSV)活化诱导的Toll样受体3(TLR3)的干预作用,探讨其治疗RSV肺炎可能的免疫学机制。方法:RSV感染体外培养的RAW264.7细胞,采用金欣口服液含药血清进行干预,并设利巴韦林阳性对照,24h...目的:通过研究金欣口服液含药血清对呼吸道合胞病毒(RSV)活化诱导的Toll样受体3(TLR3)的干预作用,探讨其治疗RSV肺炎可能的免疫学机制。方法:RSV感染体外培养的RAW264.7细胞,采用金欣口服液含药血清进行干预,并设利巴韦林阳性对照,24h后收集细胞,Real time RT-PCR法测定TLR3 mRNA的表达变化;激光共聚焦显微镜观察免疫荧光细胞化学染色法处理的各组细胞TLR3表达水平;ELISA法检测各组细胞培养上清中白细胞介素-6(IL-6)含量,在核酸及蛋白水平探讨金欣口服液含药血清抗RSV感染的作用机制。结果:RSV感染RAW264.7细胞后24h,细胞中TLR3 mRNA和蛋白表达水平以及细胞培养上清中IL-6表达明显升高(P<0.01),而金欣组TLR3及IL-6表达均显著低于RSV感染组(P<0.01,P<0.05),且效果优于利巴韦林组(P<0.01,P<0.05)。结论:金欣口服液含药血清能下调RSV活化诱导的TLR3及其下游炎症因子IL-6的高表达,推测其为金欣口服液抗RSV感染的机制之一。展开更多
基金supported by the National Natural Science Foundation of China(Nos.82073232,81700769,81641028)the Traditional Chinese Medicine Research Fund of Hubei Provincial Administration of Traditional Chinese Medicine(No.ZY2021M005)+5 种基金the Hubei Science&Technology Department Foundation(Nos.2020CFB558,2018ACA162)the Key Projects of Hubei Education(No.D20202103)the Department of Biomedical Research Foundation,Hubei University of Medicine(No.HBMUPI201803)the Advantages Discipline Group(medicine)Project in Higher Education of Hubei Province(Nos.2022XKQT3,2022XKQY1)the Innovative Research Program for Graduates of Hubei University of Medicine(Nos.YC2022022,YC2020039,YC2020002)Science and Technology Research Project of Hubei Education Department(No.B2019110).
文摘Acute lung injury(ALI)is a prevalent and severe clinical condition characterized by inflammatory damage to the lung endothelial and epithelial barriers,resulting in high incidence and mortality rates.Currently,there is a lack of safe and effective drugs for the treatment of ALI.In a previous clinical study,we observed that Jinyinqingre oral liquid(JYQR),a Traditional Chinese Medicine formulation prepared by the Taihe Hospital,Affiliated Hospital of Hubei University of Medicine,exhibited notable efficacy in treating inflammation-related hepatitis and cholecystitis in clinical settings.However,the potential role of JYQR in ALI/acute respiratory distress syndrome(ARDS)and its anti-inflammatory mechanism remains unexplored.Thus,the present study aimed to investigate the therapeutic effects and underlying molecular mechanisms of JYQR in ALI using a mouse model of lipopolysaccharide(LPS)-induced ALI and an in vitro RAW264.7 cell model.JYQR yielded substantial improvements in LPS-induced histological alterations in lung tissues.Additionally,JYQR administration led to a noteworthy reduction in total protein levels within the BALF,a decrease in MPAP,and attenuation of pleural thickness.These findings collectively highlight the remarkable efficacy of JYQR in mitigating the deleterious effects of LPS-induced ALI.Mechanistic investigations revealed that JYQR pretreatment significantly inhibited NF-κB activation and downregulated the expressions of the downstream proteins,namely NLRP3 and GSDMD,as well as proinflammatory cytokine levels in mice and RAW2647 cells.Consequently,JYQR alleviated LPS-induced ALI by inhibiting the NF-κB/NLRP3/GSDMD pathway.JYQR exerts a protective effect against LPS-induced ALI in mice,and its mechanism of action involves the downregulation of the NF-κB/NLRP3/GSDMD inflammatory pathway.
文摘Objective: To investigate the protective effectof Qidongyixin Oral Liquidon cultured rat cardiomyocytes infected withCVB 3 . Methods:Monolayer culture of spontaneously contracting rat heart cells were obtained from new born SD rats and seeded into culture plates. Results:Chronic Pulmonary Emphysema was lightened,Qidongyixin Oral Liquidcould inhibit the release of cardiac cytosolic enzymes-lactic acid dehydrogenase and glutamic-pyruvic transaminase. Conclusion: Qidongyixin Oral Liquidhas protective effects on viral myocarditis.
文摘Objective:The effect of prevention and treatment of Xinkang oral liquid(心康口服液,XKOL)on experimental coxsackievirus B_(3)(CVB_(3))myocarditis mice model were investigated.Methods:The mice were inoculated intraperitoneally with 0.3 ml of 105 TCID 50 of CVB_(3)to induce acute viral myocarditis model.These mice were divided into model control group(Group A),prevention high dosage group(Group B)and prevention low dosage group(Group C),treatment high dosage group(Group D)and treatment low dosage group(Group E),respectively.In addition,XKOL control group(Group F)and normal control group(Group G)were not infected with CVB_(3)intraperitoneally.The administration of XKOL in Group B and C began 2 days before virus infection.All animals were sacrificed on day 20 for evaluation.Results:Histological examination showed extensive myocardial necrosis and cell infiltration in most of Group A mice,but necrosis and cell infiltration were less severe in Group B,C,D and E mice.Thymus weight in Group B,C,D and E mice were heavier and less cell depletion occurred than those in Group A.Conclussion:The XKOL could effectively inhibit myocardial CVB_(3)replication,reduce the myocardial inflammatory response,lower incidence rate of myocarditis and prevent the disease associated lymphoid organ atrophy in this animal models.
文摘目的:通过研究金欣口服液含药血清对呼吸道合胞病毒(RSV)活化诱导的Toll样受体3(TLR3)的干预作用,探讨其治疗RSV肺炎可能的免疫学机制。方法:RSV感染体外培养的RAW264.7细胞,采用金欣口服液含药血清进行干预,并设利巴韦林阳性对照,24h后收集细胞,Real time RT-PCR法测定TLR3 mRNA的表达变化;激光共聚焦显微镜观察免疫荧光细胞化学染色法处理的各组细胞TLR3表达水平;ELISA法检测各组细胞培养上清中白细胞介素-6(IL-6)含量,在核酸及蛋白水平探讨金欣口服液含药血清抗RSV感染的作用机制。结果:RSV感染RAW264.7细胞后24h,细胞中TLR3 mRNA和蛋白表达水平以及细胞培养上清中IL-6表达明显升高(P<0.01),而金欣组TLR3及IL-6表达均显著低于RSV感染组(P<0.01,P<0.05),且效果优于利巴韦林组(P<0.01,P<0.05)。结论:金欣口服液含药血清能下调RSV活化诱导的TLR3及其下游炎症因子IL-6的高表达,推测其为金欣口服液抗RSV感染的机制之一。
