Singh Rajeev, Rai Umesh
Department of Zoology, University of Delhi, Delhi 110 007, India.
Dev Comp Immunol. 2008;32(4):330-8. doi: 10.1016/j.dci.2007.06.005. Epub 2007 Jul 9.
In this in vitro study, the role of beta-endorphin in the control of phagocytic and cytotoxic activities of fish splenic phagocytes was investigated. Further, the involvement of specific opioid receptor was explored. beta-Endorphin stimulated phagocytosis, whereas inhibited nitric oxide production as assessed by nitrite release. However, it had concentration-related biphasic effects on superoxide production, stimulatory at low and inhibitory at high concentration. Naltrexone, non-selective opioid receptor antagonist, antagonized the effect of beta-endorphin on phagocyte functions. Moreover, CTAP, selective mu-receptor antagonist, completely blocked the effect of beta-endorphin on phagocytosis and nitrite release. With regard to superoxide production, CTAP blocked the stimulatory effect of beta-endorphin at low concentration, while the inhibitory effect at high concentration was completely antagonized by selective delta-receptor antagonist, NTI. In conclusion, beta-endorphin acting via mu-receptor stimulated phagocytosis and inhibited nitric oxide production, while its biphasic effect on superoxide production seems to be mediated by mu- and delta-receptors.
在这项体外研究中,研究了β-内啡肽在控制鱼类脾脏吞噬细胞的吞噬和细胞毒性活性中的作用。此外,还探讨了特异性阿片受体的参与情况。β-内啡肽刺激吞噬作用,而通过亚硝酸盐释放评估发现其抑制一氧化氮的产生。然而,它对超氧化物的产生具有浓度相关的双相作用,低浓度时具有刺激作用,高浓度时具有抑制作用。非选择性阿片受体拮抗剂纳曲酮拮抗了β-内啡肽对吞噬细胞功能的影响。此外,选择性μ受体拮抗剂CTAP完全阻断了β-内啡肽对吞噬作用和亚硝酸盐释放的影响。关于超氧化物的产生,CTAP阻断了β-内啡肽在低浓度时的刺激作用,而高浓度时的抑制作用则被选择性δ受体拮抗剂NTI完全拮抗。总之,β-内啡肽通过μ受体发挥作用,刺激吞噬作用并抑制一氧化氮的产生,而其对超氧化物产生的双相作用似乎是由μ受体和δ受体介导的。