Comparison of different puncture methods in C57BL/6 mouse tail veins / 中国比较医学杂志

Objective Four different methods were examined to identify a safer and more reliable method for tail vein punctures in C57BL/6 mice. Methods In total,320 mice were randomly divided into four groups: a blank group, incandescent lamp baking method group,three-line method group,and combined method group. Blood samples were taken from the left or right peripheral vein of puncture mice. Puncture success rate of each group was recorded. SPSS 13.0 software was used to compare statistical difference among groups. Results Compared with the blank group,success rates of the other three methods were significantly higher(P < 0.001). Further, the three-line method was better than the incandescent lamp baking method(P< 0.001). The success rate of the combined method was significantly higher than the three-line and incandescent lamp baking methods(P< 0.001). Conclusions The combined method greatly improved the success rate of tail vein punctures in C57BL/6 mice. This method is more reliable and should be more widely used in the future.

Effect of hydrogen inhalation on p38 MAPK activation in rats with lipopolysaccharide- induced acute lung injury / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the effect of hydrogen inhalation on lipopolysaccharide (LPS)-induced acute lung injury (ALI) and the underlying molecular mechanisms.</p><p><b>METHODS</b>Thirty-two male SD rats were randomly divided into 4 groups (n=8), namely the normal saline group (SA), saline with 2% hydrogen gas inhalation group (SH group), ALI group, and ALI with hydrogen inhalation group (LH group). In the two ALI groups, ALI was induced by intraperitoneal injection of 15 mg/kg LPS. Treatments with inhalation of 2% hydrogen gas for 6 h was administered after the injection of LPS or saline. The concentrations of tumor necrosis factor-α (TNF-α) in the lung tissue and serum were examined with ELISA. The expression of p38 MAPK in the lung tissue was detected by Western blotting..</p><p><b>RESULTS</b>Hydrogen inhalation decreased the expression of p-p38 MAPK in the lung tissue, and significantly reduced TNF-α content in the lung tissue and serum of rats with ALI.</p><p><b>CONCLUSION</b>Hydrogen inhalation can decrease the expression of TNF-α in the lung tissue and serum, and this effect may be related with reduced p38 MAPK expression and inhibition of p38 MAPK activation.</p>

Inhibitory effect of resveratrol on ischemia reperfusion-induced cardiocyte apoptosis and its relationship with PI3K-Akt signaling pathway / 中国中药杂志

<p><b>OBJECTIVE</b>To study the effect of resveratol on ischemia reperfusion-induced cardiocyte apoptosis and its relationship with PI3K-Akt signaling pathway.</p><p><b>METHOD</b>Fifty male SD rats were divided randomly into five groups: the control group (SH group), the ischemia reperfusion group (I/R group), the resveratol pretreatment group (Res group), the resveratol pretreatment + wortmannin group (Res +Wom group) and the ischemia reperfusion + wortmannin group (I/R + Wom group). The myocardial ischemia model was established by ligating left coronary artery for 45 min followed by 120 min reperfution, in order to observe the contents of NOS and NO. Cardiac myocyte apoptosis was determined by terminal deoxynueleotidyl transferase-mediated dUTP nick end labeling (TUNEL). Bcl-2 and Bax proteins were detected by immunohistochemistry. The t-Akt and p-Akt signaling protein expressions were determined by Western blotting analysis.</p><p><b>RESULT</b>Compared with the I/R groups and the Res + Wom group, the Res group showed significant increase in the expressions of NOS, NO, Bcl-2 protein and p-Akt and notable decrease in cardiocyte apoptosis and Bax/Bcl-2. The difference of above indicators showed a statistical significance (P<0.05). Furthermore, above changes can be blocked by wortmannin, a specific blocker of PI3K-Akt signaling pathway, indicating a statistical significance in their changes (P<0.05).</p><p><b>CONCLUSION</b>Resveratol can inhibit the ischemia reperfusion-induced cardiocyte apoptosis, in which PI3K-Akt signaling pathway gets involved.</p>

Effects of hydrogen gas on myocardial injury in rats with endotoxemia / 中华麻醉学杂志

Objective To investigate the effects of hydrogen gas on the myocardial injury in rats with endotoxemia.Methods Forty-eight healthy male Sprague-Dawley rats,weighing 200-220 g,were randomly divided into 4 groups (n =12 each ):control group (group C ),hydrogen gas control group (group HC ),endotoxemia group (group E) and hydrogen gas + endotoxemia group (group LH).Endotoxemia was induced by intraperitoneal lipopolysaccharide (LPS) 20 mg/kg in groups E and LH,while the equal volume of normal saline was given in groups C and HC.After LPS administration,the rats were exposed to the air containing 2％ hydrogen gas for 6 h in groups HC and LH,and the rats were exposed to the air for 6 h in groups C and E.Blood samples were taken from the abdominal aorta after 6 h inhalation of hydrogen gas to determine the serum level of cTnI.The hearts were then removed to determine the content of TNF-α and IL-6 and expression of phosphorylated nuclear factor κB ( NF-κB) inhibitory protein (p-IκB-α) and p38 mitogen-activated protein kinase (p-p38MAPK) in the myocardial tissues.Results Compared with group C,no significant change was found in the levels of cTnI,TNF-α and IL-6 and expression of p-IκB-α and p-p38MAPK in group HC ( P ＞ 0.05),and the levels of cTnI,TNF-α and IL-6 were significantly increased and the expression of p-IκB-α and p-p38MAPK was up-regulated in groups E and LH ( P ＜ 0.05).Compared with group E,the levels of cTnI,TNF-α and IL-6 were significantly decreased and the expression of p-IκB-α and p-p38MAPK was down-regulated in group LH ( P ＜ 0.05).Conclusion Hydrogen gas can reduce the myocardial injury in rats with endotoxemia,and inhibition of the p38MAPK and NF-κB pro-inflammatory pathway and reduction of the inflammatory response of myocardial tissues are involved in the mechanism.

Role of cadiocyte connexin 43 in mito-KATp channel mediated cardioprotection against ischemia-reperfusion injury induced by sevoflurane preconditioning in isolated rat hearts / 中华麻醉学杂志

Objective To evaluate the role of cadiocyte connexin 43 (Cx43) in mito-KATP channel mediated cardioprotection against ischemia-reperfusion(I/R) injury induced by sevoflurane preconditioning in isolated rat hearts.Methods Forty hearts from male adult SD rats weghing 200-250 g were excised and perfused in a Langendorff apparatus with K-H solution with 95 ％ O2-5 ％ CO2 at 36.5-37.5 ℃.Their hearts were randomly divided into 5 groups (n =8 each): control group (group C),group I/R,sevoflurane preconditioning group (group S),sevoflurane preconditioning + 5-HD group (group SH) and 5-HD group (group H).Myocardial I/R was induced by occlusion of the anterior descending branch of left coronary artery (LAD) for 30 min followed by 120 min reperfusion.After 10 min of equilibration,group C received continuous perfusion and LAD was exposed but not occluded.Group I/R received continuous perfusion for 30 min and LAD was occluded.In group S,SH and H,3％ sevoflurane,3 ％ sevoflurane mixed with 100μmmol/L 5-HD and 100 tmmol/L 5-HD was added into K-H solution to perfuse for 15 min respectively.After that,the hearts were washed by K-H solution for 15 min.HR,left ventricular systolic pressure ( LVSP),left ventricular diastolic pressure (LVDP) and ± dp/dtmax were recorded before administration (T0),immediately after administration (T1),immediately before ischemia ( T2 ),at 30 min of ischemia (T3) and 120 min of reperfusion (T4).At the end of reperfusion,left ventricular tissue was removed for determination of myocardial infarct size and expression of Cx43 and phosphor Cx43 (p-Cx43) by immunohistochemistry and Western blot respectively.Results Compared with group C,HR,LVSP and ± dp/dtmax were significantly decreased,LVDP was increased and the expression of Cx43 and p-Cx43 were down-regulated in groups I/R,SH and H (P ＜ 0.05).Compared with group I/R,HR,LVSP and ± dp/dtmax were significantly increased,LVDP and myocardial infarct size decreased,and the expression of Cx43 and p-Cx43 up-regulated in group S ( P ＜ 0.05),no significant difference was found in groups S + H and H( P ＞ 0.05 ).Conclusion Sevoflurane preconditioning can open mito-KATP channel,promote cadiocyte Cx43 phosphorylation,attenuate I/R injury in isolated rat hearts.

Effects of doxazosin enantiomers on blood pressure and urinary bladder function in anesthetized rats / 中国药理学通报

Aim To study effects of intraduodenal administration of S-doxazosin, R-doxazosin and rac-doxazosin on the carotid blood pressure and urinary bladder function in anesthetized rats. Methods The various parameters of carotid blood pressure, heart rate, vesical micturition pressure, intercontraction interval in anesthetized rats were recorded with an ADInstruments PowerLab/8s data recording and analysis system, and the vesical micturition volume was measured simultaneously. Results S-Doxazosin, R-doxazosin and rac-doxazosin administered intraduodenally decreased the systolic blood pressure, diastolic blood pressure and mean arterial blood pressure significantly in anesthetized rats in a dose-dependent manner. The inhibition of mean arterial pressure by S-doxazosin, R-doxazosin and rac-doxazosin at 1.0 mg?kg-1 was 23.5%?4.6%, 38.5%?8.9% and 42.6%?7.5%, respectively. The ED30 values of decreasing mean arterial blood pressure by S-doxazosin, R-doxazosin and rac-doxazosin were (2.0?0.8),(0.6?0.7) and (0.6?0.5) mg?kg-1,respectively. S-Doxazosin had a weaker inhibitory effect on the carotid blood pressure compared with R-doxazosin and rac-doxazosin, but no significantly different effect was observed between R-doxazosin and rac-doxazosin on the carotid blood pressure. rac-Doxazosin produced a significant inhibition on the heart rate at the dosage from 0.1 mg?kg-1 to 3.0 mg?kg-1 in a dose-dependent manner, but S-doxazosin and R-doxazosin reduced the heart rate only at 3.0 mg?kg-1. S-Doxazosin, R-doxazosin and rac-doxazosin administered intraduodenally decreased the vesical micturition pressure dose-dependently in anesthetized rats. The maximal inhibition of vesical micturition pressure by S-doxazosin, R-doxazosin and rac-doxazosin was 13.4%?5.7%, 14.5%?11.0% and 10.9%?7.6%, and their inhibitory potency on the vesical micturition pressure was not significantly different each other. R-Doxazosin, however, decreased the intercontraction interval and vesical micturition volume significantly compared with S-doxazosin, but S-doxazosin and rac-doxazosin did not significantly affect the intercontraction interval and vesical micturition volume. Conclusion In comparison with R-doxazosin and rac-doxazosin, S-doxazosin administered intraduodenally remains the beneficial action on vesical micturition pressure and relieves the adverse effects on blood pressure, heart rate and intercontraction interval in anesthetized rats.