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Objective To study the effects of human uriilary kallikrein(HUK)on the number of apoptotic cells and the expressions of Bcl-2 and Bax proteins in rats after focal cerebral ischemia and reperfusion(FCIR) injury. Methods Eighty-four Spmque-Dawley(SD)male rats were randomly divided into sham-operated group(n=12),ischemia-reperfusion group(n=36),and HUK-treated group (n=36). Transient focal cerebml ischemia models were established by middle cerebml artery occlusion.Six rats were chosen from sham-operated group,ischemia-reperfusion group,and HUK-treated group for measuring infarct sizes.The rest were used to evaluate neurologic fhnction impaiment and measure the nunlber of apoptotic cells and Bcl-2 or BaX protein positive cells in cerebral cortex with TUNEL and immunohistochemistry.The latter 2 groups were subdivided into 6,12,24,72,168 h reperfusio groups (each n=6). Results The neurologic function impairmlent score,the infarct sizes,the apoptotic cells and the expression of Bax protein of HUK-treated group at different time points (except 168 h group)significantly decreased compared wilh those of ischemia-reperfsion group (p＜0.05).The expression of Bcl-2 protein of HUK-treated group at different time points(except 168 h group) remarkably increased compared with that of ischemia-reperfusion group(P＜0.05). Conclusions HUK can excrt a protection against FCIR injury, maybe through up-regulating Bcl-2 and down-regulating Bax protein in the initial 3 d of FCIR injury to decrease the number of apoptotic cells
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Objective To explore the effect of human urinary kallikrein on the expression of VEGF in focal cerebral ischemia-reperfusion rats. Methods Fifty-six male SD rats were randomly divided into sham operated group (n=8), saline group (n=24) and human urinary kallikrein group (n=24).The latter 2 groups were made into middle cerebral artery occlusion (MCAO) models, and subdivided into 5 subgroups according to the five time points of 6, 12, 24, 72 h, and 7 d after ischemia-reperfusion.We used the methods of nerve function scales, TTC staining, infarct size estimation, detection with light microscope to evaluate the MCAO rat models at different time points, and analyzed the changes of the expression of VEGF in the center and the periphery of infarcts at different time points by immunohistochemical methods. Results The degrees of neurological impairment in the rats of human urinary kallikrein group were lighter than those of saline group (P＜0.05). The average infarct size of rats at 24 h was (53 261.96±7 326.75) μm3 in human urinary kallikrein group, (92 715.84±13 755.44) μm3 in saline group, and the difference between the 2 groups was significant (P＜0.05). The expression of VEGF in the rats of human urinary kallikrein group was higher than that of saline group at different time points (P＜0.05). Conclusions Human urinary kallikrein has neuroprotective effect after ischemia reperfusion injury, and can promote the levels of VEGF expression.
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Objective:To study the reasons and preventive measure of the effect of human urinary kallikrein on blood pressure in the treatment of acute cerebral infarction.Method:Documents about the effect of human urinary kallikrein on blood pressure of pre-clinical study and the phaseⅠ-Ⅲclinical trials were collected and analyzed in combination with the related information of the phaseⅣclinical trial from our hospital.Result:The rate and concentration of medication in combination with ACEI were the reasons for the effect of human urinary kallikrein on blood pressure.Conclusion:Controlling the rate and concentration of medication and forbidding the combined use of ACEI from the 72hr before the medication and the 24hr after it can prevent hypotension caused by human urinary kallikrein.
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OBJECTIVE:To observe the effects of different concentration of human urinary kallikrein on blood pressure when used for acute cerebral infarction. METHODS: By a non-randomized historical control study,the blood pressure variation of 34 patients on day one after treatment with low concentration (0.06%) of human urinary kallikrein was observed,the occurrence of hypotension in this group was compared with that of another 47 patients (control) treated with high concentration (0.3%) of human urinary kallikrein. RESULTS: The reduction of blood pressure in low concentration group was less obvious than in the high-concentration group. However,hypotension was noted in both groups when angiotensin-converting enzyme inhibitor (ACEI) hypotensive drugs were used concomitantly. CONCLUSION: Human urinary kallikrein for acute cerebral infarction can transiently down-regulate blood pressure slightly,but its effect on blood pressure can be lowered by suitable reduction of its concentration;at any concentration,it can result in hypotension if used in combination with ACEI.