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Objective To explore the effect of tissue kallikrein 1 (KLK1) on mitochondrial function after cardiac ischemia/reperfusion (I/R) injury and its mechanism. Methods After KLK1 overexpression by KLK1 recombinant adenovirus infection, the cardiac I/R rat model was established by ligation of left anterior descending coronary artery and reperfusion. The cardiac infarction area and the apoptosis of cardiomyocytes were detected. The mitochondria were isolated from injured myocardial tissues, and mitochondrial functions (mitochondrial superoxide production, membrane potential and ATP production) determined. The neonatal rat cardiomyocytes were isolated and infected with KLK1 recombinant adenovirus to achieve KLK1 overexpression, and then hypoxia/reoxygenation (H/R) cell model was established. The H/R cells were treated with the media containing bradykinin receptor type 1 (B1R) antagonist R715 or bradykinin receptor type 2 (B2R) antagonist HOE140. The cell viability was determined with MTT assay, and the mitochondrial functions were observed. Results In I/R rats, KLK1 overexpression could alleviate the cardiac injury, and decrease infarction area and cell apoptosis (all P0.01) in cardiac ischemic risk area; moreover, KLK1 overexpression could improve mitochondrial dysfunction, decrease mitochondrial peroxide production, and increase mitochondrial membrane potential and ATP production (all P0.01). In vitro cardiomyocyte model, KLK1 overexpression could also attenuate cardiomyocyte injury (P0.01) and mitochondrial dysfunction (P0.05, P0.01), which could be inhibited by B2R antagonist HOE140. Conclusion KLK1 mitigates mitochondrial dysfunction after cardiac I/R injury, which may be an important mechanism of its cardioprotective effect.
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<p><b>OBJECTIVE</b>To investigate the effects of intragastric administration of Clostridium butyricum in regulating serum uric acid, lipopolysaccharides (LPS), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in rats with hyperuricemia rats.</p><p><b>METHODS</b>Forty SD rats were randomized into 4 equal groups, namely the normal control group, hyperuricemia model group, benzbromarone (3 mg/kg daily) intervention group and live Clostridium butyricum group (1.5×10CFU/day). Except for those in the control group, the rats were subjected to intragastric administration of yeast extract and oteracil potassium once daily for 12 weeks to induce hyperuricemia with corresponding treatments. The changes in serum uric acid, lipopolysaccharides , IL-6 and TNF-α in each group were detected.</p><p><b>RESULTS</b>The serum level of uric acid was significantly higher in rats fed with high-purine diet than in the control rats (P<0.01), demonstrating the successful establishment of hyperuricemia models. In rats with hyperuricemia, serum uric acid level was positively correlated with the levels of LPS, IL-6 and TNF-α, and their serum levels decreased significantly and progressively with time in Benzbromarone group and Clostridium butyricum group. Benzbromarone was more effective in decreasing serum uric acid in the rats, while Clostridium butyricum produced a stronger effect in down-regulating the inflammatory mediators.</p><p><b>CONCLUSION</b>Chronic inflammatory reaction exists in rats with hyperuricemia. Intragastric administration of Clostridium butyricum can effectively decrease serum uric acid level and inhibit the inflammatory cytokines, and thus contributes to immune homeostasis in the intestines.</p>
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<p><b>OBJECTIVE</b>To investigate the expressions of survivin and GRIM-19 in prostatic cancer tissue and their clinical implications.</p><p><b>METHODS</b>We detected the expressions of survivin and GRIM-19 in the tissues of normal prostate (NP), benign prostate hyperplasia (BPH) and prostate cancer (PCa) using immunohistochemical staining, RT-PCR and Western blot, and processed the data by SPSS12.</p><p><b>RESULTS</b>The positive rates of survivin expression were 6.25% , 18.18% and 90.62% in NP, BPH and PCa (P < 0.01), while those of GRIM-19 were 87.50%, 81.82% and 9.37% , respectively (P < 0.01). Semiquantitative RT-PCR and immunohistochemical staining showed that both survivin mRNA and survivin expressions were highly positive in PCa but negative in NP and BPH. Western blot exhibited that the survivin protein was expressed strongly in PCa but weakly in NP and BPH, while the GRIM-19 protein was expressed just contrariwise (P < 0.01).</p><p><b>CONCLUSION</b>The expressions of survivin and GRIM-19 may be closely correlated with the pathogenesis of prostate cancer.</p>