Objective To investigate whether sodium tanshinone ⅡA sulphonate ( STS) treatment attenuates pulmonary edema of seawater drowning ( PE-SWD) , and examine the effects of STS on Na-KATPase(NKA) in PE-SWD. Methods Thirty-six rats were randomly divided into there groups, ie. a normal group ( NG) , a seawater group ( SG) , and a STS treatment group ( TG) . The rat model of PE-SWD was established by seawater instillation. PaO2 , histological changes of lungs, lung wet /dry weight ratio ( W/D) ,pulmonary microvascular permeability ( PMVP) , and NKA activity were detected. Western blot were used to test the effects of STS on NKA-α1 expression. Results Seawater instillation decreased PaO2 and the expression of NKA, while increased W/D ratio and PMVP. At 2 h after seawater instillation, the PaO2 in the TG group were significantly higher than those in the SG group, and peaked at 4 h after seawater instillation.Histological examination showed that there were hemorrhage, edema, markedly thickened alveolar wall, and infiltration of inflammatory cells in alveolar spaces in the SG group, but lung injury was significantly alleviated in the TG group. W/D ratio and PMVP in the TG group were significantly lower than those in the SG group. Additionally, NKA activity and NKA-α1 expression were significantly higher in the TG group than those in the SG group. Conclusion STS treatment can attenuate pulmonary edema of seawater drowning which may be related with up-regulating Na-K-ATPase activity and expression.
目的:研究丹参酮ⅡA(Tan ⅡA)对急性早幼粒细胞白血病(APL)细胞株NB4细胞诱导的血管内皮细胞株(ECV304)促凝活性(PCA)的影响,并对其机制作初步探讨。方法:(1)分别用1.0μg/mL TanⅡA、0.3μg/mLATRA、0.01%DMSO、PRMI1640处理NB4细胞24、48和72h,取其上清液作为条件培养基(hNB4-CM)。将这些CM分别与ECV304细胞在37oC共同孵育0、4、8和12h,用反复冻融法制备ECV304细胞裂解液,采用一期凝血法测定其PCA;采用ELISA法测定条件培养基中的TNF-α 。(2)ECV304细胞与1.0μg/mL TanⅡA及TanⅡA 72h-NB4-CM 在37oC共同分别孵育6、12、24和48h,并以ATRA和DMSO分别作为阳性和阴性对照,用上述相同方法测定ECV304细胞裂解液的PCA。结果:(1)1.0 μg/mL Tan ⅡA可以诱导NB4细胞分化,其作用NB4细胞的培养基有一定的升高ECV304细胞PCA的作用,该作用在孵育4h时达高峰,之后ECV304细胞PCA逐渐下降。与0.3μg/mL ATRA的作用无统计学差异(Pgt;0.05)。(2)1.0 μg/mL的TanⅡA对TanⅡA72h-NB4-CM促ECV304细胞PCA有抑制作用,其强度随作用时间增加而增加,与1.0μmol/L ATRA比较,Pgt;0.05。(3)TanⅡA作用NB4细胞的培养基中TNF-α浓度,在作用前7h内随作用时间增加而增加,与0.3μg/mL ATRA比较无差异(Pgt;0.05)。结论:Tan ⅡA能诱导NB4细胞分化,后者在分化过程中释放的TNF-α可能与ECV304细胞PCA活性升高有关;Tan-ⅡA又能抑制Tan-ⅡA-NB4-CM增强ECV304细胞PCA的作用。
ObjectiveTo investigate the therapeutic effects of different doses of tanshinone ⅡA microemulsion on radioactive lung injury. MethodsSeventy-two Wistar rats were randomly divided into a healthy control group,a model group,a liposome microemulsion treatment group,a tanshinone ⅡA microemulsion high-dose group,a tanshinone ⅡA microemulsion middle-dose group,and a tanshinone ⅡA microemulsion low-dose group.Radiation-induced lung injury model was established by irradiation of radiotherapy instrument.In addition to the control group,other groups received 6MV X radiation with one dosage of 22Gy.Four rats in each group were sacrificed on 7th,14th,and 28th day,respectively.Lung tissues were sampled to analyze the pathological changes by HE staining and the Smad7 mRNA expression by RT-PCR.The level of glutathione(GSH)in peripheral blood was determined by ultraviolet spectrophotometric method. ResultsIn the model group and four treatment groups,lung tissue biopsy showed the pathological changes gradually from pulmonary alveolitis to fibrosis.The level of Smad7 mRNA in lung tissue and GSH in peripheral blood were higher in the high-dose group,the middle-dose group and the low-dose group than those in the model group at all time points(P<0.05),and were highest in the high-dose group.There was no significant differences in the level of Smad7 mRNA in lung tissue and GSH in peripheral blood between the liposome microemulsion treatment group and the middle-dose group. ConclusionTanshinone ⅡA microemulsion has treatment effect on lung injury in a dose dependent manner.
Cardiovascular disease is one of the diseases with the highest morbidity and mortality in the world. Tanshinone ⅡA is one of the main active components of Salvia miltiorrhiza, which can significantly improve heart function. In this paper, the mechanisms of cardiovascular protection by tanshinone ⅡA are reviewed, including reducing myocardial apoptosis, inhibiting inflammatory reaction, improving atherosclerosis, and inhibiting myocardial fibrosis and antioxidant stress, and the related clinical research of tanshinone ⅡA is evaluated, so as to provide reference for the following research and clinical application of tanshinone ⅡA in cardiovascular system.