目的评价逍遥散合生脉饮加减结合西医常规疗法治疗干眼症的疗效。方法将符合入选标准的76例干眼症患者按随机数字表法分为2组,每组38例。对照组给予西医常规疗法治疗,观察组在对照组基础上结合逍遥散合生脉饮加减治疗。2组均治疗4周。...目的评价逍遥散合生脉饮加减结合西医常规疗法治疗干眼症的疗效。方法将符合入选标准的76例干眼症患者按随机数字表法分为2组,每组38例。对照组给予西医常规疗法治疗,观察组在对照组基础上结合逍遥散合生脉饮加减治疗。2组均治疗4周。分别于治疗前后进行自觉症状评分,并依据角膜荧光素染色试验(fluorescent test, FL)、泪膜破裂时间(breakup time of tear film, BUT)、基础泪液分泌试验(schirmer I test, SIT)评价泪膜稳定性;采用ELISA法检测泪液中IL-1b、IL-6及TNF-a含量,评价临床疗效。结果观察组总有效率为92.9%(65/70)、对照组为76.4%(55/72),2组比较差异有统计学意义(Z=-2.991,P=0.002)。治疗后,观察组SIT[(6.9±0.8)mm比(4.3±0.5)mm,t=3.751]、BUT[(10.5±1.6)s比(6.4±0.8)s,t=4.228]均高于对照组(P<0.05),FL[(0.9±0.1)分比(1.4±0.2)分,t=3.208]评分均低于对照组(P<0.05);观察组干涩、异物感、视疲劳、畏光及视物模糊评分均低于对照组(t值分别为3.559、4.015、4.119、3.983、4.120,P值均<0.05);泪液中IL-1b、IL-6及TNF-a水平均低于对照组(t值分别为11.887、8.028、8.112,P值均<0.001)。结论逍遥散合生脉饮加减结合西医常规疗法可提高干眼症患者的泪膜稳定性,减轻眼表局部炎症反应,改善临床症状,提高临床疗效。展开更多
The present study was designed to investigate whether a combination of four effective components derived from Sheng-mai san(SMXZF; ginsenoside Rb1: ginsenoside Rg1: DT^(–1)3: Schizandrol A as 6 : 9 : 4 : 5) could att...The present study was designed to investigate whether a combination of four effective components derived from Sheng-mai san(SMXZF; ginsenoside Rb1: ginsenoside Rg1: DT^(–1)3: Schizandrol A as 6 : 9 : 4 : 5) could attenuate hydrogen peroxide(H_2O_2)-induced injury in PC12 cells, focusing on the Akt and MAPK pathways. The PC12 cells were exposed to H_2O_2(400 mmol·L^(–1)) for 1 h in the presence or absence of SMXZF pre-treatment for 24 h. Cell viability was measured by MTT assay. The efflux of lactate dehydrogenase(LDH), the intracellular content of malondialdehyde(MDA), the activities of superoxide dismutase(SOD), and caspase-3 were also determined. Cell apoptosis was measured by Hoechst 33342 staining and Annexin V-FITC/PI staining method. The expression of Bcl-2, Bax, cleaved caspase-3, Akt, and MAPKs were detected by Western blotting analyses. SMXZF pretreatment significantly increased the cell viability and SOD activity and improved the cell morphological changes, while reduced the levels of LDH and MDA at the concentrations of 0.1, 1 and 10 μg·m L^(–1). SMXZF also inhibited H_2O_2-induced apoptosis in PC12 cells. Moreover, SMXZF reduced the activity of caspase-3, up-regulated the protein ratio of Bcl-2 and Bax and inhibited the expression of cleaved caspase-3, p-Akt, p-p38, p-JNK and p-ERK1/2 in H_2O_2-induced PC12 cells. Co-incubation of Akt inhibitor or p38 inhibitor partly attenuated the protection of SMXZF against H_2O_2-injured PC12 cells. In conclusion, our findings suggested that SMXZF attenuated H_2O_2-induced injury in PC12 cells by inhibiting Akt and MAPKs signaling pathways, which might shed insights on its neuroprotective mechanism.展开更多
Sheng-Mai-San(SMS), a well-known Chinese medicinal plant formula, is widely used for the treatment of cardiac diseases characterized by deficiency of Qi and Yin syndrome. A mouse chronic intermittent hypoxia(CIH) mode...Sheng-Mai-San(SMS), a well-known Chinese medicinal plant formula, is widely used for the treatment of cardiac diseases characterized by deficiency of Qi and Yin syndrome. A mouse chronic intermittent hypoxia(CIH) model was established to mimic the primary clinical features of deficiency of Qi and Yin syndrome. Mice experienced CIH for 28 days(nadir 7% to peak 8% oxygen, 20 min per day), resulting in left ventricle(LV) dysfunction and structure abnormalities. After administration of SMS(0.55, 1.1, and 5.5 g·kg-1·d-1) for four weeks, improved cardiac function was observed, as indicated by the increase in the ejection fraction from the LV on echocardiography. SMS also preserved the structural integrity of the LV against eccentric hypotrophy, tissue vacuolization, and mitochondrial injury as measured by histology, electron microscopy, and ultrasound assessments. Mechanistically, the antioxidant effects of SMS were demonstrated; SMS was able to suppress mitochondrial apoptosis as indicated by the reduction of several pro-apoptotic factors(Bax, cytochrome c, and cleaved caspase-3) and up-regulation of the anti-apoptosis factor Bcl-2. In conclusion, these results demonstrate that SMS treatment can protect the structure and function of the LV and that the protective effects of this formula are associated with the regulation of the mitochondrial apoptosis pathway.展开更多
文摘目的评价逍遥散合生脉饮加减结合西医常规疗法治疗干眼症的疗效。方法将符合入选标准的76例干眼症患者按随机数字表法分为2组,每组38例。对照组给予西医常规疗法治疗,观察组在对照组基础上结合逍遥散合生脉饮加减治疗。2组均治疗4周。分别于治疗前后进行自觉症状评分,并依据角膜荧光素染色试验(fluorescent test, FL)、泪膜破裂时间(breakup time of tear film, BUT)、基础泪液分泌试验(schirmer I test, SIT)评价泪膜稳定性;采用ELISA法检测泪液中IL-1b、IL-6及TNF-a含量,评价临床疗效。结果观察组总有效率为92.9%(65/70)、对照组为76.4%(55/72),2组比较差异有统计学意义(Z=-2.991,P=0.002)。治疗后,观察组SIT[(6.9±0.8)mm比(4.3±0.5)mm,t=3.751]、BUT[(10.5±1.6)s比(6.4±0.8)s,t=4.228]均高于对照组(P<0.05),FL[(0.9±0.1)分比(1.4±0.2)分,t=3.208]评分均低于对照组(P<0.05);观察组干涩、异物感、视疲劳、畏光及视物模糊评分均低于对照组(t值分别为3.559、4.015、4.119、3.983、4.120,P值均<0.05);泪液中IL-1b、IL-6及TNF-a水平均低于对照组(t值分别为11.887、8.028、8.112,P值均<0.001)。结论逍遥散合生脉饮加减结合西医常规疗法可提高干眼症患者的泪膜稳定性,减轻眼表局部炎症反应,改善临床症状,提高临床疗效。
基金supported by National Natural Science Foundation of China(No.81274004)2011 Program for Excellent Scientific and Technological Innovation Team of Jiangsu Higher Educationthe Priority Academic Program Development of Jiangsu Higher Education Institutions
文摘The present study was designed to investigate whether a combination of four effective components derived from Sheng-mai san(SMXZF; ginsenoside Rb1: ginsenoside Rg1: DT^(–1)3: Schizandrol A as 6 : 9 : 4 : 5) could attenuate hydrogen peroxide(H_2O_2)-induced injury in PC12 cells, focusing on the Akt and MAPK pathways. The PC12 cells were exposed to H_2O_2(400 mmol·L^(–1)) for 1 h in the presence or absence of SMXZF pre-treatment for 24 h. Cell viability was measured by MTT assay. The efflux of lactate dehydrogenase(LDH), the intracellular content of malondialdehyde(MDA), the activities of superoxide dismutase(SOD), and caspase-3 were also determined. Cell apoptosis was measured by Hoechst 33342 staining and Annexin V-FITC/PI staining method. The expression of Bcl-2, Bax, cleaved caspase-3, Akt, and MAPKs were detected by Western blotting analyses. SMXZF pretreatment significantly increased the cell viability and SOD activity and improved the cell morphological changes, while reduced the levels of LDH and MDA at the concentrations of 0.1, 1 and 10 μg·m L^(–1). SMXZF also inhibited H_2O_2-induced apoptosis in PC12 cells. Moreover, SMXZF reduced the activity of caspase-3, up-regulated the protein ratio of Bcl-2 and Bax and inhibited the expression of cleaved caspase-3, p-Akt, p-p38, p-JNK and p-ERK1/2 in H_2O_2-induced PC12 cells. Co-incubation of Akt inhibitor or p38 inhibitor partly attenuated the protection of SMXZF against H_2O_2-injured PC12 cells. In conclusion, our findings suggested that SMXZF attenuated H_2O_2-induced injury in PC12 cells by inhibiting Akt and MAPKs signaling pathways, which might shed insights on its neuroprotective mechanism.
基金supported by National Natural Science Foundation of China(No.81303076)the Clinical Science and Technology Project of Department of Science and Technology of Jiangsu Province(No.BL2012060)the Eleventh Five-Year Technology Support Project(No.2008BAI51B03)
文摘Sheng-Mai-San(SMS), a well-known Chinese medicinal plant formula, is widely used for the treatment of cardiac diseases characterized by deficiency of Qi and Yin syndrome. A mouse chronic intermittent hypoxia(CIH) model was established to mimic the primary clinical features of deficiency of Qi and Yin syndrome. Mice experienced CIH for 28 days(nadir 7% to peak 8% oxygen, 20 min per day), resulting in left ventricle(LV) dysfunction and structure abnormalities. After administration of SMS(0.55, 1.1, and 5.5 g·kg-1·d-1) for four weeks, improved cardiac function was observed, as indicated by the increase in the ejection fraction from the LV on echocardiography. SMS also preserved the structural integrity of the LV against eccentric hypotrophy, tissue vacuolization, and mitochondrial injury as measured by histology, electron microscopy, and ultrasound assessments. Mechanistically, the antioxidant effects of SMS were demonstrated; SMS was able to suppress mitochondrial apoptosis as indicated by the reduction of several pro-apoptotic factors(Bax, cytochrome c, and cleaved caspase-3) and up-regulation of the anti-apoptosis factor Bcl-2. In conclusion, these results demonstrate that SMS treatment can protect the structure and function of the LV and that the protective effects of this formula are associated with the regulation of the mitochondrial apoptosis pathway.
