[Role of protein kinase C in protecting rats against pulmonary ischemia reperfusion injury through opening of mitochondrial ATP sensitive potassium channel].

OBJECTIVE: To investigate the effect of opening of mitochondrial ATP-sensitive potassium channel on inducing lung protection against ischemia reperfusion injury (I/R) and the role of PKC in the protective effect. METHODS: Fifty-six rats were divided into six groups, including sham-operation group, I/R group, DE (diazoxide) +I/R group, 5-HD (5-hydroxydecanoic acid) +DE+I/R group, CHE (chelerythrine) +DE+I/R group and 5-HD +PMA (phorbol 12-myristate 13-acetate)+ I/R group. Pulmonary I/R injury rat models were established by 45 min of left hilar clipping followed by 180 min of reperfusion. Morphological changes in lung tissues were detected by HE staining. The wet-to-dry weight ratio of lung tissues was evaluated. Cytochrome C expression in lung tissues was assessed by immunohistochemical staining. TUNEL was used to determine apoptosis. Protein kinase C (PKC) activity in lung tissues was assessed by PepTag non-radioactive assay. RESULTS: Compared with I/R group, the lung tissue morphology of the rats in the DE+I/R group was preserved well and the wet-to-dry weight ratio, expression of cytochrome C and apoptosis index decreased significantly (P < 0.05). The PKC activity in the lung tissues of the rats in the DE+ I/R group increased dramatically. Both pretreatment with 5-HD and CHE blocked the protective effect induced by DE preconditioning. There were no differences between 5-HD+PMA+I/R group and I/R group in the above indicators except for PKC activation. These results showed that blocking of mitochondrial ATP-sensitive potassium channel by 5-HD did not protect lung from ischemia reperfusion injury even though PKC were activated. CONCLUSION: Opening of mitochondrial ATP-sensitive potassium channel plays an essential protective role in pulmonary ischemia reperfusion injury. The pulmonary protection appears to be dependent on PKC activation.

[Protective effect of tetramethylpyrazine and L-arginine on rats with acute myocardial infarction].

OBJECTIVE: To compare the protective effects of tetramethylpyrazine (TMP) alone and TMP and L-arginine (TMP-LA) combination on rats with acute myocardial infarction (AMI), and to explore its mechanism. METHODS: The rat model of AMI was established by via caudal vein injection of pituitrin. Experimental animal groups of normal, model, TMP treated and TMP-LA (via abdominal cavity and caudal vein respectively) treated groups were established. Expression of P- and E-selectin, serum creatine phosphokinase (CK) and troponin T (TnT), and marrow peroxidase (MPO) concentration in myocardial tissue were determined by immunohistochemical stain. RESULTS: As compared with the normal group, serum CK and TnT level, and MPO concentration in myocardial tissue were significantly higher in the model group (P < 0.01), with P- and E-selectin significantly up-regulated (P < 0.01). As compared with the model group, the above-mentioned parameters in the TMP or TMP-LA treated group was significantly lower (P < 0.05). CONCLUSION: Combined use of TMP and LA showed obvious synergism in treating AMI, by way of multi-link inhibition on expression of adhesive factors and decrease of leucocyte infiltration.