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Objective:To explore the effect of tanshinone ⅡA on myocardial remodeling in ischemia/reperfusion (I/R)-induced heart failure of rodent model.Methods:① In vivo, 30 SD rats were randomly divided into sham operation, heart failure and tanshinone ⅡA treatment group, with 10 rats in each group. The I/R model was established by ligating the left coronary artery until ST segment elevation for 30 minutes, then the ligation was removed for 2 hours as reperfusion. In the sham operation group, the rat chest was opened without artery ligation. Three days after model establishment, tanshinone ⅡA (10 mg/kg) were given intraperitoneal injected in tanshinone ⅡA group for 9 weeks. In the other two groups, normal saline was administrated in the same way. The behavioral manifestations of the rats in each group were observed; hemodynamic indexes were evaluated; Masson staining was performed to observe the degree of myocardial fibrosis; enzyme linked immunosorbent assay (ELISA) was used to detect the content of Galectin-3 in myocardial tissue; quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was used to detect the expressions of collagenⅢ, collagenⅠ, matrix metalloproteinase 2 (MMP-2) and tissue inhibitor of metalloproteinase (TIMP-1). ② In vitro, rats primary cardiac fibroblasts were extracted and isolated, and divided into blank control group, angiotensinⅡ group (7-10 mmol/L angiotensinⅡ) and angiotensinⅡ+ tanshinoneⅡA group (7-10 mmol/L angiotensinⅡ+ 5-10 mmol/L tanshinone ⅡA). At 24 hours and 48 hours of culture, the cell proliferation in each group was detected by methyl thiazolyl tetrazolium (MTT); the expressions of collagenⅢ, collagenⅠ, MMP-2 and TIMP-1 were detected by qRT-PCR; the content of Galectin-3 in cardiac fibroblasts was detected by ELSIA. Results:① In vivo, the rats' activity status, hair conformity and food intake were ranked from good to bad in order of sham operation group, tanshinone ⅡA group and heart failure model group. Compared with the sham-operated group, the heart rate (HR) of the rats in the heart failure model group was significantly decreased and the heart function was significantly impaired. The mRNA and protein expression of collagenⅠ, collagenⅢ, TIMP-1 and Galectin-3 content were significantly increased, while the mRNA and protein expression of MMP-2 were significantly decreased. Compared with the heart failure model group, rats in the tanshinone ⅡA group showed significantly higher HR and improved cardiac function, significantly lower mRNA expression of collagenⅠ and collagenⅢ, significantly lower mRNA and protein expression of TIMP-1 and Galectin-3, and significantly higher mRNA and protein expression of MMP-2, and the most obvious changes were in the 9th weeks of modeling [collagenⅠ mRNA (2 -ΔΔCt): 4.70±1.19 vs. 10.21±1.62, collagenⅢ mRNA (2 -ΔΔCt): 3.03±0.46 vs. 13.84±1.93, TIMP-1 mRNA (2 -ΔΔCt): 1.90±0.19 vs. 4.55±0.43, TIMP-1/GAPDH: 0.33±0.04 vs. 0.67±0.05, Galectin-3 (ng/L): 489.93±79.30 vs. 821.72±94.09, MMP-2 mRNA (2 -ΔΔCt): 0.37±0.07 vs. 0.03±0.01, MMP-2/GAPDH: 0.69±0.09 vs. 0.21±0.04, all P < 0.05]. Masson staining showed that myocardial tissue fibrosis was obvious in the heart failure group, and the degree of fibrosis in the tanshinoneⅡA group was reduced. ② In vitro, compared with the blank control group, the proliferation rate, collagenⅠ, collagen Ⅲ and TIMP-1 expression and Galectin-3 content of myocardial fibroblasts were significantly increased, and MMP-2 expression was significantly decreased in the angiotensin group at 24 h and 48 h of culture. Compared with the angiotensin group, the proliferation rate of cardiac fibroblasts and the expression of collagenⅠ, collagen Ⅲ and TIMP-1 and the content of Galectin-3 were significantly decreased, and the expression of MMP-2 mRNA was significantly increased in the angiotensin + tanshinone ⅡA group, and the most significant changes were at 48 hours of culture [proliferation rate: (57.0±3.7)% vs. (67.0±2.4)%, collagenⅠmRNA (2 -ΔΔCt): 551.43±67.10 vs. 871.48±12.25, collagenⅢ mRNA (2 -ΔΔCt): 233.76±18.73 vs. 385.51±31.35, TIMP-1 mRNA (2 -ΔΔCt): 238.69±17.37 vs. 351.84±26.17, Galectin-3 (ng/L): 283.76±28.73 vs. 415.51±31.35, MMP-2 mRNA (2 -ΔΔCt): 108.54±12.10 vs. 51.47±6.25, all P < 0.05]. Conclusion:Tanshinone ⅡA can improve cardiac function, inhibit myocardial fibrosis and improve myocardial remodeling in rats with I/R-induced heart failure.
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Objective To investigate the effect of lung protective and ventilatory management strategies for brain death donors on eligibility and availability of lungs for transplantation.Method The clinical data of two brain dead patients who accepted lung protective ventilatory management strategies from Feb.2015 to Mar.2015 were retrospectively analyzed.Two cases of brain-dead patients,due to severe cerebral trauma,accepted the aggressive lung protective ventilatory management strategies and airway management for 9 days and 4 days respectively.PaO2/FiO2,chest imaging manifestations,surface of the lung harvested and pulmonary rehabilitation of recipients after operation were observed.Result Two lung recipients were liberated from ventilation and pulmonary function improved significantly after double lung transplantation.Conclusion The application of lung protective ventilatory strategies in potential organ donors with brain death can increase the number of eligible and harvested lungs.
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Objective To investigate the coagulant function of Thrombomodulin-Protein C-EPCR System in rats with hemorrhagic shock in virto study.Methods In this study,30 rats were divided into three groups,with each group 10 rats:control group,the sham shock group,hemorrhagic shock group.Hemorrhagic shock model was subjected to computer-controlled arterial hemorrhage to 40 mm Hg for 60 min The rat blood serum samples were obtained from rats in sham shock group and shock group after maintaining 3 hours,and fetal bovine serum (FBS) was used as control group.Then medium contained fore-mentioned serums cultured with SV40-transformed aortic rat endothelial cells for 6 hours,12 hours and 18hours.The messenger RNA (mRNA) expression of thrombmodulin (TM),Endothelial cell protein C receptor in the SV40-transformed aortic rat endothelial cells which were treated with serums were detected by reverse-transcription polymerase chain reaction.Results Compared to control group,SVARECs were incubated for 6hrs with shock serum,the mRNA expression of TF,TM and t-PA was significantly higher,and continued elevating at the time of 18 hours (P ＜ 0.01).Conclusions Serums from hemorrhagic shock rats upregulate TMmRNA EPCRmRNA expression on the endothelial cells surface.It is suggested that Thrombomodulin-Protein C-EPCR System pay a key role of anticoagulation,the protection of endothelial function.
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ObjectiveTo investigate the influence of Tanshinone Ⅱ A on the expression of HMGB1 in rats with cerebral ischemia-reperfusion (I/R) injury and its neural function protection.MethodsThe 32 male SD rats were randomly (random number) divided into 4 groups (8 rats per group):Sham group,I/R group,group with low dose of Tanshinone Ⅱ A ( TaLD group) and group with high dose of Tanshinone Ⅱ A (TaHD group).The cerebral I/R models were established by the method of right middle cerebral artery occlusion (MCAO).Cerebral infarct volume was detected by TTC staining.Apoptotic cell and apoptotic index were calculated by Tunnel assay.The HMGB1 levels in brain and serum was detected by Western blot and ELISA.Calmodulin (CaM) activity and malondialdehyde (malondiadehyde,MDA) content in the brain were also detected.ResultsCompared with the Sham group,the volume of cerebral infarction,the number of apoptotic cells,CaM activity,MDA content,HMGB1 levels in the brain tissue and serum in group I/R,TaLD group and TaHD group increased significantly (P ＜ 0.01 ).Compared with the group I/R,the volume of cerebral infarction,the number of apoptotic cells,CaM activity,MDA content and the HMGB1 levels in brain tissue and serum in TaLD groupand TaHDgroup decreased significantly (P ＜ 0.01 ).The difference of the above index between TaLD groupand TaHDgroup was significant ( P ＜ 0.01 ).ConclusionsTan Ⅱ A could reduce the cerebral ischemic reperfusion injury in rats which was likely related with decreasing the inflammatory response in the late stage via HMGB1.