ABSTRACT
<p><b>OBJECTIVE</b>To investigate the expressions of leptin and its receptor in the epididymis of experimental varicocele (EV) rats.</p><p><b>METHODS</b>Forty male Sprague-Dawley rats were randomly divided into four groups: 4-week EV (n = 12), 8-week EV (n = 12), 4-week control (n = 8), and 8-week control (n = 8). EV models were established by partial ligation of the left renal vein. The expressions of leptin and its receptor in the rat epididymis were measured by immunohistochemistry, and their mRNA expressions determined by real-time quantitative PCR.</p><p><b>RESULTS</b>The expressions of leptin and its receptor in the epididymis were significantly higher in the 4- and 8-week EV groups than in the 4- and 8-week control groups (P < 0.01), with no significant difference between the two EV groups (P > 0.05). So were their mRNA expressions in the former two than in the latter two groups (P < 0.01), with no significant difference between the former two (P > 0.05).</p><p><b>CONCLUSION</b>The expressions of leptin and its receptor are markedly increased in the epididymis of varicocele rats. Leptin may be involved in the mechanisms of varicocele inducing male infertility.</p>
Subject(s)
Animals , Male , Rats , Disease Models, Animal , Epididymis , Metabolism , Leptin , Metabolism , Rats, Sprague-Dawley , Receptors, Leptin , Metabolism , Varicocele , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To study the protective effect of dl-tetrahydropalmatine(dl-THP) on liver injury induced by carbon tetrachloride (CC4) in mice.</p><p><b>METHOD</b>Mice were administracted with dl-tetrahydropalmatine ip 20, 40 mg x kg(-1) daily for 9 d respectively, and then actue liver injury model was induced by 0.1% carbon tetrachloride ip 20 mL x kg(-1). The mice were killed 17 h after injection ip of CCl4, serum alanine and aspartate aminotransferase (ALT and AST) activity were measured, and maleic dialdehyde (MDA) and superoxide dismutase(SOD) activity in liver were detected.</p><p><b>RESULT</b>dl-THP significantly reduced the level of serum ALT and AST, inhibited lipoperxidation in liver, while increased SOD activity in liver tissue. Degeneration of hepatocytes was obviously prevented in mice treated with dl-THP, and the liver histological structure was well maintained.</p><p><b>CONCLUSION</b>dl-THP has inhibitory effects on liver injury induced by CCl4 in mice. The mechanisms may be related with its effects of reducing lipid peroxidation product.</p>