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1.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-552298

ABSTRACT

Objectives In order to study the endogenous opioid polypeptides involved in pathogenesis of epidemic encephalitis-B and the clinical therapeutic efficacy.Methods ①Leucine-enkephalin,?-endophin and Dynorphin levels in plasma and and CSF of patients with epidemic encephalitis-B during critical stage and convalescent stage were measured by radio-immunoassay.②Naloxone therapeutic efficacy in patients with epidemic encephalitis-B were investigated.Results Opioid polypeptides levels In plasma and CSF were significantly higher in critical stage and dropped to normal levels in convalescent stage.③We demonstrated that endogenous opioid polypeptides special antagnoist agent-Naloxone was a very important therapy agent for epidemic encephalitis-B patients.Therapy group efficacy was significantly better than control group.Conclusions These results demonstrate that endogenous opioid polypeptides involves in the physiopathologic changes of epidemic encephalitis-B.

2.
Chinese Journal of Hypertension ; (12): 130-133, 2001.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-411161

ABSTRACT

Aim To investigate the effects of angiotensin Ⅱ(AngⅡ),AT1 receptor antagonist losartan and AT2 receptor antagonist PD123177 on protein synthesis rate and AT1 receptor mRNA expression in cultured neonatal rat cardi ac myocytes.  Methods The protein synthesis rate in cultured cardiac myocytes w as determined by the3H-leucine incorporation,AT1 receptor mRNA expressi on of cardiac myocytes was assessed by reverse transcription-polymerase chain reaction(RT-PCR).  Results AngⅡ increased the  3H-leucine incorporation in cultured cardiac myocytes in a dose dependent manner,losartan but not PD12317 7 could significantly inhibit AngⅡ induced protein synthesis,;AT1 receptor mRNA expression was upregulated after AngⅡ,and inhibited by losartan,but not PD123177.  Conclusion AngⅡ can induce cardiac myocytes hypertrophy via upregulating AT1 receptor,and AT1 receptor antagonist can decrease AT1 rec eptor expression,reduce cardiac myocytes hypertrophy.

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