The role of JNK in apoptosis of renal tubular epithelial cells in diabetic rats with fluctuant high blood glucose / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To explore the signal transduction mechanisms of apoptosis in renal tubular epithelial cells in diabetic rats with fluctuant high blood glucose.</p><p><b>METHODS</b>Healthy SD rats were randomly divided into 3 groups: normal control group (A), stable high blood glucose group (B) and fluctuant high blood glucose group (C). Diabetic rats were induced by intraperitoneal injection of streptozotocin (STZ, 65 mg/kg), and the fluctuant high blood glucose animal model was induced by intraperitoneal injection of ordinary insulin and glucose at different time point every day. The superoxide dismutase (SOD) activity and the content of malonaldehyde (MDA) in renal tissue homogenate were detected with colorimetry. The protein expression of Nox4 and JNK were examined by immunohistochemistry and Western blot. Apoptosis was assessed by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling (TUNEL).</p><p><b>RESULTS</b>After 12 experimental weeks, significantly increased cell apoptosis, up-regulation of Nox4 and P-JNK expression in renal tubular epithelial cells were observed in B and C groups compared with those in A group. The MDA content increased and SOD activity decreased in renal tissue in B and C groups. Above effects were more obviously shown in C group.</p><p><b>CONCLUSION</b>Fluctuant high blood glucose induced more apoptosis of renal tubular epithelial cell than stable high blood glucose in diabetic kidney, which might be related to the activation of JNK signal transduction pathway.</p>

Effects of cyclosporine A on pneumocyte apoptosis with lung ischemia/reperfusion injury in rats / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To investigate the effects of cyclosporine A (CsA), a powerful inhibitor of mitochondrial permeability transition pore (MPTP), on pneumocyte apoptosis, the release of cytochrome C and the activity of caspase-3 after lung ischemia/reperfusion, and explore the mechanisms.</p><p><b>METHODS</b>Single lung in situ ischemia/reperfusion animal model was used. 30 SD rats were randomly divided into three groups (n = 10): sham (S) group, ischemia/reperfusion (I/R) group and cyclosporine A (CsA) group. Apoptosis of pneumocyte was assessed by TUNEL method, cytochrome C (CytC) in cytoplasm was detected by immunohistochemistry techniques, and the activity of caspase-3 was measured with spectrophotometer.</p><p><b>RESULTS</b>The content of CytC in cytoplasm, the activity of caspase-3, and the value of apoptosis index (AI) in ischemia/reperfusion group were evidently higher than that in S group (P < 0.01). CsA suppressed apoptosis as well as CytC release and caspase-3 activity (P < 0.01).</p><p><b>CONCLUSION</b>CsA can prevent the release of cytochrome C, block the apoptosis of pneumocyte accordingly maybe by closing the MPTP.</p>

Effect of ligustrazine and L-arginine on function of mitochondria in myocardium after ischemia/reperfusion injury of myocardium in rabbits / 中国应用生理学杂志

<p><b>AIM</b>To study the effect of ligustrazine (LGT) and L-arginine(L-Arg)on function of mitochondria in myocardium after myocardial ischemia/reperfusion injury (MI/RI).</p><p><b>METHODS</b>50 rabbits were randomly divided into five groups (n=10): Control group(A), MI/R group(B), MI/R + LGT group (C), MI/R+ L-Arg group (D), MI/R+ LGT + L-Arg group (E). The mitochondrial respiratory function, Ca2+ concentration ([Ca2+]m), malondialdehyde (MDA) content and superoxide dismutase (SOD) activity were deter mined. Meanwhile, the contents of ATP and EC in the myocardial tissue were measured, respectively.</p><p><b>RESULTS</b>It was found that mitochondrial respiratory control rate (RCR), state 3 (ST3), SOD in C, D, E group were higher than those of B group, state 4 (ST4), [Ca2+]m, MDA were lower than those of B group, ATP and EC levels of myocardial tissue were higher than those in B group; and there were not significant differences between E and A group of above.</p><p><b>CONCLUSION</b>LGT and IL-Arg can improve function of mitochondria in myocardium after ischemia/reperfusion injury of myocardium in rabbits by decreasing oxygen free radical level and Ca" overload in the mitochondria.</p>

Effect of ligustrazine on the expression and activity of heme oxygenase-1 in the pulmonary ischemia/reperfusion injury in rabbits / 中国应用生理学杂志

<p><b>AIM</b>To explore the effect of ligustrazine injection on the expression of heme oxygenase-1 (HO-1) in rabbits with pulmonary ischemia/reperfusion injury after.</p><p><b>METHODS</b>Single lung ischemia/reperfusion injury animal model was used in vivo. Twenty rabbits were randomly divided into two groups( n = 10, in each), pulmonary ischemia/reperfusion injury (I/R) group and I/R + ligustrazine injection (LGT) group. The tissue slides were stained by immunohistochemistry (IHC) and in situ hybridization (ISH) for HO-1 to detect the expression of HO-1 in lung and to analyze the absorbance, wet to dry ratio of lung tissue weight (W/D) and the injured alveoli rate (IAR) were measured at 180 minutes after lung reperfusion. Meanwhile the lung tissue slide was prepared for electron microscopic observation at 180 minutes after reperfusion.</p><p><b>RESULTS</b>HO-1 expression was upregulated in two groups in the pulmonary endothelial cells, part of pulmonary vascular smooth muscle cells, extima of vessels and epithelial cells of airway, the absorbance was 0.168 +/- 0.016 (0.148 +/- 0.013), 0.186 +/- 0.014 (0.158 +/- 0.012) respectively.The LGTI group showed higher absorbance than those of the I/R group (P < 0.01), lower W/D and IAR values than those of the I/R group (P < 0.01) significantly and lighter abnormal changes of the lung tissue in morphology than those of the I/R group.</p><p><b>CONCLUSION</b>Ligustrazine injection possesses notable protective effects on I/R in rabbits by increasing the expression of HO-1 in lung.</p>