Zhang Q, Li T, Huang Y
Department of Surgery, First Teaching Hospital, Beijing Medical University.
Zhonghua Zheng Xing Shao Shang Wai Ke Za Zhi. 1995 May;11(3):205-8.
Mechanisms of postburn immunosuppression are complicated and remain unclear. In the present experiment the effect of linoleic acid hydroperoxide (LOOH) on lymphocytes was evaluated in vitro, and then the changes in postburn lipid peroxide (LPO) levels and lymphocyte functions were measured, in order to investigate the mechanism of immunosuppression following burn.
Proliferation and IL-2 production and LPO of lymphocytes were assayed after the incubation with LOOH for in vitro study. On day 6 after induction of 11%-12% TBSA full-thickness burn, the animals were sacrificed, and proliferation and IL-2 production of splenic lymphocytes, LPO levels of the plasma, livers and spleens were measured.
LOOH inhibited proliferation and IL-2 production and induced lipid peroxidation of lymphocytes in vitro, and Vit E could attenuate the effects of LOOH. LPO levels increased and proliferation and IL-2 production decreased after burn, but those changes in Vit E or SOD group showed no statistical significance compared with normal control group.
Enhancement of lipid peroxidation and increased LPO after burn may be one of the mechanisms of postburn immunosuppression.
烧伤后免疫抑制的机制复杂且尚不清楚。在本实验中,体外评估了氢过氧化亚油酸(LOOH)对淋巴细胞的影响,然后测定烧伤后脂质过氧化物(LPO)水平和淋巴细胞功能的变化,以探讨烧伤后免疫抑制的机制。
体外研究中,用LOOH孵育后测定淋巴细胞的增殖、白细胞介素-2生成及LPO。在诱导11%-12%体表面积全层烧伤后第6天,处死动物,测定脾淋巴细胞的增殖和白细胞介素-2生成、血浆、肝脏和脾脏的LPO水平。
LOOH在体外抑制淋巴细胞增殖和白细胞介素-2生成并诱导淋巴细胞脂质过氧化,维生素E可减弱LOOH的作用。烧伤后LPO水平升高,增殖和白细胞介素-2生成减少,但维生素E或超氧化物歧化酶组的这些变化与正常对照组相比无统计学意义。
烧伤后脂质过氧化增强及LPO增加可能是烧伤后免疫抑制的机制之一。