Clinical study of Xiaoyaosan and Shengmaiyin combined with conventional western medicine in the treatment of xerophthalmia / 国际中医中药杂志

Objective To evaluate the effect of Xiaoyaosan and Shengmaiyin combined with conventional western medicine for xerophthalmia.Methods A total of 76 xerophthalmia patients who met the criteria were divided into two groups according to random number table,with 38 cases in each group.The control group was treated with routine western medicine,while the observation group was treated with Xiaoyaosan combined with Shengmaiyin on the basis of the control group.Both groups were treated for 4 weeks.Before and after treatment,the symptoms were scored,and the tear film stability was evaluated according to the results of fluorescent test (FL),breakup time of tear film (BUT) and schirmer Ⅰ test (SIT).The contents of IL-1β,IL-6 and TNF-α in tear were detected by ELISA,and the clinical efficacy was evaluated.Results The total effective rate was 92.9％ (65/70) in the observation group and 76.4％ (55/72) in the control group,and there was significant difference between the two groups (Z=-2.991,P=0.002).After treatment,the SIT (6.9 ± 0.8 mm vs.4.3 ± 0.5 mm,t=3.751),BUT (10.5 ± 1.6 s vs.6.4 ± 0.8 s,t=4.228) in the observation group were significantly higher than those in the control group (P＜0.05).The FL score (0.9 ± 0.1 vs.1.4 ± 0.2,t=3.208) in the observation group was significantly lower than that of the control group (P＜0.05).The scores of aningeresting,foreign body sensation,visual fatigue,photophobia and visual blur in the observation group were significantly lower than those in the control group (t were 3.559,4.015,4.119,3.983,4.120,all Ps＜0.05).The levels of IL-1β,IL-6 and TNF-α in tear were significantly lower than those in control group (t were 11.887,8.028,8.112,all Ps＜0.001).Conclusions The Xiaoyaosan combined with Shengmaiyin can improve tear film stability,relieve local ocular surface inflammation and improve clinical symptoms in patients with xerophthalmia.

A combination of four effective components derived from Sheng-mai san attenuates hydrogen peroxide-induced injury in PC12 cells through inhibiting Akt and MAPK signaling pathways / 中国天然药物

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-13: Schizandrol A as 6 : 9 : 4 : 5) could attenuate hydrogen peroxide (H2O2)-induced injury in PC12 cells, focusing on the Akt and MAPK pathways . The PC12 cells were exposed to H2O2 (400 μmol·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·mL(-1). SMXZF also inhibited H2O2-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 H2O2-induced PC12 cells. Co-incubation of Akt inhibitor or p38 inhibitor partly attenuated the protection of SMXZF against H2O2-injured PC12 cells. In conclusion, our findings suggested that SMXZF attenuated H2O2-induced injury in PC12 cells by inhibiting Akt and MAPKs signaling pathways, which might shed insights on its neuroprotective mechanism.

Sheng-Mai-San attenuates contractile dysfunction and structural damage induced by chronic intermittent hypoxia in mice / 中国天然药物

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.