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Aim To study the effects of salidroside on the complement components in MCAO rats and to further explore the mechanism of neuroprotection of salidroside. Methods Forty-five healthy male Sprague-Dawley rats were randomly divided into sham operation (Sham) group, model (MCAO) group, and salidroside (MCAO + Sal) group. Rats were administered salidroside, or vehicle, daily for 6 days, after middle cerebral artery occlusion( MCAO) 2 h and reperfusion 1 h. The protein expressions of C3 and brain tissue mitochondrial Bax, Bcl-xl were detected by Western blot. The mRNA expressions of Clqa, Clqb, Clqc, C2, C3, C3a, C4a, C5a, Cfh, Cfd were detected by qPCR. Gene chip technology was used for detection. The expressions of C3 and NeuN were detected by im-munofluorescence. Results Compared with MCAO group, salidroside could reduce the protein expression of Bax protein in mitochondria and promote the expression of Bcl-xL protein after salidroside treatment. By gene chip cluster analysis and qPCR detection, salidroside could inhibit the expression of complement-related genes such as Clqa, Clqb, Clqc, C2, C3, C3a, C4a, C5ar, Cfh and Cfd mRNA. According to West-em blot and immunofluorescence, salidroside inhibited the expression of C3 and promoted the expression of NeuN. Conclusions Salidroside can inhibit the complement component, especially the action of the complement central component C3, exerting neuroprotective effects on MCAO rats.
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Objective To investigate the effect of hydrogen sulfide (H 2 S or NaHS)on myo-cardial ischemia reperfusion injury induced in type 2 diabetic rats in vivo and the role of AMP-activated protein kinase (AMPK)signal pathway.Methods The induced type 2 diabetic rat models were anesthetized,left thoracotomy were performed.All the models were randomly divided into six groups (n = 14):group Sham;group IR:the left anterior descending artery was ligated 30 min, reperfused for 4 hours;group CC:prior to thoracotomy,compound c was intraperitoneally injected 250 μg/kg,then received the same treatment as group IR;group DMSO received the same treatment as compound c group but DMSO was injected intraperitoneally as control;group NaHS:the left ante-rior descending artery was injected NaHS 0.05 mg/kg then reperfused for 4 hours;group CC +NaHS:prior to thoracotomy,compound c was intraperitoneally injected 250 μg/kg,then NaHS 0.05 mg/kg injected intravenously and reperfused 4 hours.All the rat models euthanatized,infarcted area was detected by TTC assay.The AMPK,LC3 and p62 were analyzed by Western blot.Results Com-pared with group Sham,the infarcted area and concentration of AMPK,LC3 and p62 were increased in other groups (P <0.05).Compared with group IR,the infarcted area and concentration of LC3, p62 markablely decreased in group NaHS (P < 0.05 ).Compared with group NaHS,the infarcted area and concentration of LC3,p62 significantly increased but AMPK down-regulated in group CC+NaHS (P <0.05).Conclusion Hydrogen sulfide could alleviate myocardial infraction via AMPK sig-nal pathway in type 2 diabetic rats'IR models.
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Objective Heart transplantation is an effective treatment of end-stage heart diseases and extending the time of donor heart preservation helps to make up for the shortage of donor hearts. This study was to investigate whether high-pressured mixed gas ( HPMG) of carbon monoxide and oxygen could prolong the time of donor heart preservation and its mechanisms. Methods Forty-eight C57BL/6 male mice aged 4-6 weeks were randomly divided in-to four groups of equal number:control ( the donor heart isolated but not transplanted) , immediate transplantation ( the donor heart transplanted right after isolated) , HTK-preservation ( the donor heart preserved in histidine-tryptophan-ketoglutarate solution for 24 hours after isolated, and HPMG preservation ( the donor heart preserved in an HPMG chamber with the oxygen partial pressure of 3200 hPa and carbon monoxide partial pressure of 800 hPa for 24 hours after isolated) .Another 36 recipient mice aged 6-8 weeks were randomly assigned to receive the donor heart immediately after harvested (n=12), preserved in HTK solution (n=12), or preserved in HPMG (n=12).At 2 hours after transplantation, the status of heart re-beating and cardiac function were compared among different groups of recipient mice.At 24 hours, tissues were taken from the transplanted hearts for examination of pathologic changes by HE stai-ning, detection of the apoptosis of cardiac cells by TUNEL, and determination of the expressions of microtubule-associated protein 1 light chain 3 -Ⅱ(LC3-Ⅱ) and B cell lymphoma/leukemia-2 (Bcl-2) by Western blot. Resul ts The re-beating rates of the imme-diately transplanted and HPMG-preserved hearts were significantly higher than that of the HTK-preserved ones (P<0.05).At 2 hours after transplantation, the cardiac function scores were 2.5 (2.0-2.9), 0.8 (0.5-1.0), and 4.5 (4.0-4.5) in the immediate implantation, HPMG-preservation and HTK-preservation groups respectively, with statistically significant differences between any two groups (P<0.05).The expressions of LC3-Ⅱand Bcl-2 were 2.06 ±0.29 and 0.87 ±0.18 in the HPMG-preserved heart recipients and 1.24 ±0.20 and 2.07 ±0.32 in the immediately transplanted heart recipients, both higher than 0.13 ±0.03 and 0.19 ±0.02 in the controls and 0.16 ±0.06 and 0.26 ±0.08 in the HTK-preserved heart recipients (P<0.05), the Bcl-2 higher in the HTK-pre-served heart recipients than in the controls (P<0.05), and the LC3-Ⅱ expression higher in the HPMG-preserved heart recipients than in the immediately transplanted heart recipients (P<0.05).HE staining showed that cell edema and inflammatory cell infiltration were more obvious in the HPMG-preserved heart recipients than in the controls and immediately transplanted heart recipients but less obvious than in the HTK-preserved heart recipients.The rate of cell apoptosis was dramatically increased in the HPMG-and HTK-pre-served heart recipients ([5.04 ±1.77]%and [26.72 ±5.23]%) in comparison with the controls ([1.08 ±0.56]%) (P<0.01) and immediately transplanted heart recipients ([2.13 ±1.71]%) (P<0.01) but decreased in the HPMG as compared with the HTK-preserved heart recipients (P<0.01). Conclusion High-pressured mixed gas preservation can reduce cold ischemia-reperfu-sion injury of the donor heart, which may be associated with its promotion of autophagy, provision of energy to cells, and apoptosis of cardiocytes in the donor heart.
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Objective To investigate the protective effect of adenosine A1 receptor agonist (2-chloro-N6-cyclopentyladenosine, CCPA) delayed preconditioning on myocardial ischemia reperfu-sion injury and the potential mechanism in rabbits. Methods Thirty New Zealand male white rabbits were randomly assigned to 3 groups:a control group, an I/R group, and a CCPA group. CCPA group was given CCPA 0.1 mg/kg before the myocardial ischemia. Twenty-four hours later I/R group and CCPA group underwent 40 min of coronary occlusion followed reperfusion for 2 h. At the end of the reperfusion, blood samples were taken from the arterial line for determining the plasma level of malondialdhyde and superoxide dismutase activity. The infarct size and area at risk were de-fined by Evans and TIC staining. The heart was harvested and levels of metallothionein (MT) were determined by Western blot, and ultrastructures were observed under the electron microscope. Results The MT level of CCPA group was significantly higher than that of the I/R group (P<0.05). CCPA significantly reduced the infarct size (22.1%±3.8% in the CCPA group) of the left yen-tricular area at risk as compared with the control (41.8%±4.3% in the I/R group,P<0.05). The injury of I/R group was worse than that of the CCPA group under the light microscope. CCPA group had higher superoxide dismutase and lower malondialdhyde than those of the I/R group. Con-clusion CCPA can increase the level of metallothionein during ischemia-reperfusion, which may be part of the molecular mechanism of CCPA delayed preconditioning on cardioprotection.
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AIM: To investigate the protective effects and the mechanisms of prostaglandin E1 (PGE1 ) on ischemia/reperfusion (I/R)-induced lung injury after lung transplantation in rats. METHODS: 36 SD rats were randomly divided into 3 groups ( n = 12 in each) : sham operation group ( control group) , lung transplantation (LT)group and PGE1 treatment group. PGE1 was administered to the rats through intra-venous way from 10 min before the operation to the end of the reperfusion. The wet/dry ratio of lung, lung permeability index and neutro-phil percentage were detected in bronchoalveolar lavage fluid (BALE). Superoxide dismutase (SOD) and malond-ialdehyde (MDA) of lung tissue were measured by color-imetry. Serum level of tumor necrosis factor ?(TNF?)was detected by enzyme-linked immunosorbent assay (ELISA). RESULTS: The wet/dry ratio of lung, lungpermeability index and neutrophils percentage in BALF and MDA content of lung tissue in LT group were higher than those in control group( P