Effects of Jitai tablet, a traditional Chinese medicine, on plasma adrenocorticotropic hormone and cortisol levels in heroin addicts during abstinence.

OBJECTIVES: To investigate the changes in adrenocorticotropic hormone (ACTH) and cortisol in heroin addicts given Jitai tablet treatment during abstinence. DESIGN: Double-blind, randomized, placebo-controlled clinical trial. SETTINGS/LOCATION: Drug Rehabilitation Bureau of Shanghai Police, China. PARTICIPANTS: 99 volunteers, including 69 heroin addicts and 30 healthy volunteers. INTERVENTIONS: 69 heroin addicts randomly divided into two groups: the Jitai tablet group, which comprised 34 heroin addicts given Jitai tablet treatment during abstinence, and the placebo group, which comprised 35 heroin addicts given placebo. A control group consisted of 30 sex- and age-matched healthy volunteers. OUTCOME MEASURES: ACTH and cortisol in plasma were measured in all groups at baseline and in the Jitai tablet and placebo groups on the third, seventh, and 14th days of abstinence. RESULTS: Levels of both ACTH (p<.01) and cortisol (p<.001) were significantly higher in heroin addicts at baseline than in the healthy volunteers. Jitai tablet treatment restored plasma cortisol levels to normal more rapidly than did placebo treatment (p<.05), but not ACTH levels. A positive correlation between ACTH and cortisol values at baseline (p<.01) was also found with withdrawal symptom scores and daily dosages of heroin. CONCLUSIONS: Heroin addicts could respond to Jitai tablets through changes in the hypothalamus-pituitary-adrenal axis.

Icariside II improves cerebral microcirculatory disturbance and alleviates hippocampal injury in gerbils after ischemia-reperfusion.

OBJECTIVE: the purpose of the present study was to examine the protective effect of Icariside II (IS) on cerebral microcirculatory disturbance and neuronal injury in hippocampal CA1 region induced by global cerebral I/R and the underlying mechanism. METHODS: male Mongolian gerbils (50-70 g) were subjected to bilateral common carotid arteries occlusion for 30 min and followed by reperfusion for 72 h. IS (20 mg/kg) was administered orally 2 h before ischemia and 6, 24, 48, 70 h after reperfusion. After 72 h of reperfusion, the leukocyte adhesion, albumin leakage, and velocity of RBC in the venules were determined with an upright microscope. Neuronal injury in hippocampal CA1 region was assessed by Nissl staining and the in situ TUNEL assay. Bax, Bcl-2, and cleaved caspase-3 proteins were detected by Western blot, and MDA content and complex I activity by ELISA assay in hippocampus. RESULTS: IS inhibited I/R-elicited leukocyte adhesion, albumin leakage and increased the velocity of RBC in cerebral venules. IS down-regulated Bax and cleaved caspase-3 expression, up-regulated Bcl-2 expression of hippocampus and decreased the number of TUNEL positive neurons and the neuronal loss induced by I/R in hippocampal CA1 region. In addition, IS could increase the activity of complex I and decrease the production of MDA after I/R. CONCLUSIONS: IS could alleviate the microcirculatory disturbance and neuronal injury in hippocampal CA1 region induced by global cerebral I/R, which might involve regulating complex I activity.