[Influence of beta-endorphin on function of immune system of patients with cerebral hemorrhage]

Zhonghua Yi Xue Za Zhi. 2003 Aug 25;83(16):1409-12.
[Article in Chinese]

Abstract

Objective: To study the influence of beta-endorphin (beta end) on the function of immune system of patients with cerebral hemorrhage at different stages.

Methods: Radioimmunal analysis was applied to detect the serum beta-endorphin concentration in the peripheral blood of 28 patients with cerebral hemorrhage, aged 65.5 +/- 13, 28 age-matched patients with cerebral thrombosis, and 28 sex and age-matched normal controls. Mononuclear cells from peripheral blood of these 3 kinds of subjects were cultured and then beta end 10(-8) g/L, beta end 10(-11) g/L, beta end 10(-14) g/L, or beta end 10(-11) g/L + naloxone 10(-5) g/L were added into the media respectively and the MNCs were cultured for more 24 hours (beta end 10(-8) g/L group, beta end 10(-11) g/L group, beta end 10(-14) g/L group, and beta end 10(-11) g/L + Nal group). Another MNCs were cultured without addition of beta end (beta end 0 g/L group). Then the MNCs were collected. RT-PCR was used to detect the expressions of interleukin (IL)-1beta, IL-2, IL-8 and iNOS mRNA in the MNCs.

Results: The serum beta-end level of the patients with cerebral hemorrhage at the acute stage was 129 +/- 82 ng/L, significantly lower than that of the normal controls (321 +/- 62 ng/L, P<0.01) and that of the patients with cerebral thrombosis (264 +/- 163 ng/L, P<0.05), but not significantly different from that of the patients with cerebral hemorrhage in the convalescent stage (160 +/- 72 ng/L, P>0.05). The expression of IL-1beta and the expression of IL-2 of the patients with cerebral hemorrhage at the acute stage were significantly lower than those of the patients with cerebral thrombosis and the controls (all P<0.01). The expression of IL-1beta of the patients with cerebral hemorrhage at the convalescent stage were higher than that in the acute stage, however, the difference was not significant (P>0.05). The expression of IL-2 of the patients with cerebral hemorrhage at the convalescent stage was higher than that at the acute stage (P<0.01). The expression of IL-8 and the expression of iNOS of the patients with cerebral hemorrhage at the acute stage were significantly higher than those of the patients of cerebral thrombosis and the controls (both P<0.01). The expression of IL-8 and the expression of iNOS of the patients with cerebral hemorrhage at the convalescent stage were significantly lower than those in the acute stage (both P<0.01). The expressions of IL-1beta, IL-2, IL-8, and iNOS mRNA in the peripheral blood MNCs in vitro in the beta end 10(-8) g/L group and beta end 10(-11) g/L group were significantly higher than those of the beta end 0 g/L group, beta end 10(-11) g/L group, and beta-end 10(-11) g/L + Nal 10(-5)g/L group. The expressions of IL-1beta, IL-2, IL-8, and iNOS mRNA in the peripheral blood MNCs in the beta-end 10(-11) g/L +Nal 10(-5) g/L group were higher than those of the beta end 0 g/L group, however, not significantly.

Conclusions: The endogenous beta-endorphin level of cerebral hemorrhage patients is low. The immune system function is up-regulated at the acute stage and then down-regulated. Thereafter the immune system function is invariably low. Exogenous beta-endorphin enhances the IL-1 beta, IL-2, IL-8 and iNOS mRNA expression of peripheral blood MNCS. beta-endorphin receptor antagonist naloxone blocks the positive immunoregulation by beta-endorphin.

Publication types

  • English Abstract

MeSH terms

  • Aged
  • Aged, 80 and over
  • Cerebral Hemorrhage / immunology*
  • Female
  • Humans
  • Immune System / drug effects*
  • Immune System / physiology
  • Interleukin-8 / genetics
  • Male
  • Middle Aged
  • Naloxone / pharmacology
  • Nitric Oxide Synthase / genetics
  • Nitric Oxide Synthase Type II
  • RNA, Messenger / analysis
  • beta-Endorphin / pharmacology*

Substances

  • Interleukin-8
  • RNA, Messenger
  • Naloxone
  • beta-Endorphin
  • NOS2 protein, human
  • Nitric Oxide Synthase
  • Nitric Oxide Synthase Type II