Objective:To explore the possible role of ? endorp hi n in effect of melatonin on morphine withdrawal symptoms in rats.Method:Acute model of morphine dependent rat was estalished by gradually increasing the dose of morphine through subcutaneous injections.CSF(cerebrospinal fluid)w a s got by push-pull perfusion and intracerebroventricular injection(icv)in a fixe d tuber.Concentration of ? endorphin in CSF was determined by radioimmunoassa y (RIA).Results:(1)The symptoms of natural morphine withdrawal were r e lieved significantly by icv ? Endorphin with a dose dependent manner.(2)The s y mptoms of natural morphine withdrawal were also relieved by ip melatonin.(3)The CSF ? endorphin level was significantly lower in morphine dependent rats than normal control,but that was higher in natural morphine withdrawal rats.That was also much more increased by ip melatonin in the withdrawal rats than in morphine dependent rats or normal control.Conclusion:The withdrawal symptom s could be relieved by icv ? endorphin or by ip melatonin in morphine dependetn rats.The mechanism may be partly due to the elevation of endogenous ? endorp hin level in brain of rats in withdrawal

[Objective] The present study aimed to determine the protective role of Melatonin (MT) against Acrylamide (AA)-induced testicular toxicity and the potential molecular mechanism.[Methods] The animals were randomly divided into three groups,the control group (n =12),the AA group (n =12) and the AA+MT group (n =12).The rats in the AA and AA + MT group were gavaged with AA at a dose of 15 mg/(kg · day) for 4 consecutive weeks.After 3 weeks of AA treatment,MT was intraperitoneally injected 30 minutes before AA treatment at 10 mg/(kg· day) for 1 week in the AA + MT rats.Subsequently,the mitochondrial membrane potential measurement,TUNEL assay,Western blot and electron microscopic techniques were applied in the present study.[Results] The results showed that AA could decrease the testis mitochondrial membrane potential (P ＜ 0.05) which could be recovered by MT (P ＜ 0.05).Moreover,MT induced down-regulation of Bax expression and up-regulation of Bcl-2 expression in the testis,compared with AA rats.The amelioration of testicular apoptosis was further confirmed by the TUNEL labeling.Western blot results suggested that the decreased ratios of Bcl-2/Bax and Bcl-xL/Bak in the AA group (both P ＜ 0.05) could be recovered by MT treatment (both P ＜ 0.05).The levels of Cyt-c,Casp-3,p53 and NF-κB in AA group were markedly elevated compared with the control (all P ＜ 0.05),and reduced in MT treatment group (all P ＜ 0.05).MT could relieve abnormal mitochondrial structures in the seminiferous tubule in the electron microscopic level.[Conclusion] MT may exert productive effect through its anti-apoptotic properties associated with mitochondria.