Role of HO-1 in electroacupuncture-induced alleviation of cognitive dysfunction in mice with sepsis-associated encephalopathy: relationship with mitochondrial fusion-division balance
10.3760/cma.j.cn131073.20211021.01223
- VernacularTitle:HO-1在电针减轻脓毒症相关性脑病小鼠认知功能障碍中的作用：与线粒体融合-分裂动态平衡的关系
- Author:
Rui MU
1
;
Zilei XIE
;
Jia SHI
;
Lirong GONG
;
Jianbo YU
Author Information
1. 天津市南开医院麻醉科 300100
- Keywords:
Heme oxygenase-1;
Electric stimulation therapy;
Sepsis-associated encephalopathy;
Mitochondria
- From:
Chinese Journal of Anesthesiology
2021;41(12):1506-1509
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To evaluate the role of heme oxygenase-1 (HO-1) in electroacupuncture (EA)-induced alleviation of cognitive dysfunction in mice with sepsis-associated encephalopathy (SAE) and the relationship with mitochondrial fusion-division balance.Methods:Thirty clean-grade male C57BL/6 mice (24 wide-type mice and 6 HO-1 knockout mice), aged 6-8 weeks, weighing 18-22 g, were studied.Twenty-four wide-type mice were divided into 4 groups ( n=6 each) using a random number table method: control group (group C), SAE group, SAE plus EA group (group SAE+ EA), and SAE plus sham EA group (group SAE+ SEA). HO-1 knockout mice in which EA intervention was performed after establishing SAE model served as SAE plus EA plus HO-1 knockout group (group SAE + EA+ H). Sepsis was induced by intraperitoneally injecting lipopolysaccharide 15 mg/kg.EA of Zusanli and Baihui acupoints lasting 30 min was performed after intraperitoneal injection of lipopolysaccharide once a day for 5 consecutive days in SAE+ EA and SAE+ EA+ H groups.Cognitive function was assessed using Morris water maze test before stimulation every day.The mice were sacrificed, and hippocampal tissues were removed for detection of the expression of mitofusin 2 (Mfn2), optic atrophy 1 (OPA1) and mitochondrial dynamin-related protein 1 (Drp1) by Western blot. Results:Compared with group C, the expression of Mfn2 and OPA1 was significantly down-regulated, the escape latency was prolonged, and the time spent in the target quadrant was shorted in SAE, SAE+ SEA and SAE+ EA+ H groups, and the expression of Drp1 was significantly up-regulated in SAE, SAE+ EA, SAE+ SEA and SAE+ EA+ H groups ( P<0.05). Compared with group SAE, the expression of Mfn2 and OPA1 was significantly up-regulated, the expression of Drp1 was down-regulated, the escape latency was shortened, and the time spent in the target quadrant was prolonged in group SAE+ EA ( P<0.05), and no significant change was found in the parameters mentioned above in group SAE+ SEA ( P>0.05). Compared with group SAE+ EA, the expression of Mfn2 and OPA1 was significantly down-regulated, the expression of Drp1 was up-regulated, the escape latency was prolonged, and the time spent in the target quadrant was shortened in SAE+ SEA and SAE+ EA+ H groups ( P<0.05). Conclusion:HO-1 is involved in EA-induced alleviation of cognitive dysfunction in mice with SAE, and the mechanism may be related to the regulation of mitochondrial mitochondrial fusion-division balance.
