Electroacupuncture Inhibits Neuronal Apoptosis Induced by Bilirubin Encephalopathy in SD Suckling Rats by Regulating NGB and PI3K/Akt Signaling Pathways
10.13865/j.cnki.cjbmb.2021.03.1638
- Author:
Jia-Heng HU
1
;
Li-Rong ZHANG
1
;
Yi-Ying WANG
1
;
Ling LONG
1
;
Zhi-Han HU
1
;
Wei-Min YUAN
1
;
Jing-Wen ZHAO
1
;
Shu-Juan ZHU
1
;
Juan HUANG
1
;
Guo-Ping QIU
1
;
Sheng-Wei GAN
1
;
Ping FAN
2
Author Information
1. Institute of Neurosciences, Chongqing Medical University
2. Department of Gynecology and Obstetrics, The Fifth People’s Hospital of Chongqing
- Publication Type:Journal Article
- Keywords:
apoptosis;
electroacupuncture;
Key words bilirubin encephalopathy (BE);
neuroglobin (NGB)
- From:
Chinese Journal of Biochemistry and Molecular Biology
2021;37(6):772-781
- CountryChina
- Language:Chinese
-
Abstract:
Objective In this study, electroacupuncture (EA) was used to analyze the expression changes of related proteins in neuroglobin (NGB), PI3K/AKT and apoptotic pathways in the temporal cortex of bilirubin encephalopathy (BE) rats, so as to investigate the therapeutic effect of EA on BE and the relevant mechanism of NGB in this process. Totally 39 seven-day-old SD rats were divided into Sham, BE model and BE+EA groups. The neonatal BE model was established by injecting bilirubin solution (10 μg UCB/g Weight) into the cerebellomedullary cistern, Sham group was injected with the same amount of normal saline. BE rats were treated with EA at Baihui (GV20) and Quchi (LI11) acupoints with the frequency of 2/15 Hz for 15 min. Treatment was performed 12 h before modeling, followed by treatment every 12 h, in a total of three times. HE, Nissl staining and electron microscopy (TEM) were used to observe the pathological and ultrastructural changes of nerve cells in each group. Results showed that EA treatment reduced the damage of cortical neurons of BE rats and increase the number of Nissl bodies. TEM confirmed that EA treatment could alleviate the degree of mitochondria edema. Immunofluorescence staining was used to detect the expression sites and cell types of NGB. Results showed that NGB was mainly expressed in cortical neurons. Western blotting showed that EA treatment increased the expression of NGB, PI3K (p110 alpha), pAKT (Ser473) (P< 0. 05, P< 0. 05 and P< 0. 01, respectively) and the ratio of apoptosis-related protein Bcl-2/Bax (P < 0. 001), decreased the expression of Cleaved Caspase-3 (P< 0. 05) in the temporal cortex of rats. TUNEL staining showed that EA reduced the number of apoptotic cells (BE group 186. 00±13. 86 vs BE+EA group 78. 67±11. 85, P< 0. 01) . This study confirms that EA can promote the expression of NGB in the temporal cortex of BE rats, then activate the PI3K/AKT pathway to exert its neuroprotective function and inhibit the occurrence of apoptosis. EA may become a potential treatment method for BE.
