Cong Rong San mitigates rat hippocampal neuronal apoptosis in an Al-zheimer disease model by inhibition of endoplasmic reticulum stress
10.3969/j.issn.1000-4718.2024.07.012
- VernacularTitle:苁蓉散通过抑制内质网应激减少AD模型大鼠海马神经元细胞凋亡
- Author:
Yuanqin CAI
1
,
2
;
Qinghua LONG
;
Xi WANG
;
Chuhua ZENG
Author Information
1. 湖北民族大学医学部,湖北 恩施 445000
2. 湖北民族大学风湿性疾病发生与干预湖北省重点实验室,湖北 恩施 445000
- Keywords:
Cong Rong San;
endoplasmic reticulum stress;
Alzheimer disease;
neuronal damage;
apoptosis
- From:
Chinese Journal of Pathophysiology
2024;40(7):1244-1252
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To investigate the effects of Cong Rong San(CRS)on neuronal injury and endoplasmic re-ticulum stess(ERS)in rat models of Alzheimer disease.METHODS:Sixty male Sprague-Dawley rats(2 months old)were randomly divided into control(CON),model(MOD),low-dose CRS(CRSD),medium-dose CRS(CRSZ),high-dose CRS(CRSG),and memantine hydrochloride(MJG)groups.Morris water maze experiments were used to assess learning and memory in the rats.The morphology of neurons in the CA1 region of the hippocampus was examined using HE and Nissl staining,and the morphology of the endoplasmic reticulum in hippocampal cells was observed by transmission electron microscopy.Neuronal apoptosis in the CA1 region of the hippocampus was evaluated by TUNEL staining,while Western blot was used to assess the protein expression of glucose-regulated protein 78(GRP78),B-cell lymphoma-2(Bcl-2),Bcl-2-associated X protein(Bax),caspase-3,protein kinase R-like endoplasmic reticulum kinase(PERK),p-PERK,activating transcription factor 4(ATF4)and C/EBP homologous protein(CHOP)in rat hippocampal tissues.RE-SULTS:Compared with those in the MOD group,rats in the CRSZ and CRSG groups showed improved learning and mem-ory,together with reduced hippocampal neuronal loss,PERK-ATF4-CHOP activity,and the expression of the pro-apoptot-ic proteins Bax and caspase-3,while the expression of the anti-apoptotic protein Bcl-2 was increased.CONCLUSION:Treatment with Cong Rong San was found to mitigate cognitive impairment,as well as damage and apoptosis in hippocam-pal neurons,in rat models of Alzheimer disease,possibly by inhibition of endoplasmic reticulum stress.
