D ⁃allose alleviate cerebral ischemia⁃reperfusion inj ury by down⁃regulating galectin⁃3 inhibition of the AMPK/mTOR pathway
10.19405/j.cnki.issn1000-1492.2023.09.006
- Author:
Yaowen Luo
1
,
2
,
3
,
4
,
5
;
Junkai Cheng
5
,
6
;
Min Zhang
5
,
6
;
Maorong Gou
5
,
6
;
Juan Li
5
,
6
;
Lei Zhang
5
,
6
;
Dakuan Gao
5
,
6
Author Information
1. Postgraduate Ofice , Xi &prime
2. an Medical University , Xi &prime
3. an 710068
4. Dept of Neurosurgery , Xijing Hospital , Air Force Medical University of PLA , Xi &prime
5. an 710032
6. Dept of Neurosurgery , Xijing Hospital , Air Force Medical University of PLA , Xi &prime
- Publication Type:Journal Article
- Keywords:
cerebral ischemia reperfusion injury;
D⁃allose;
Galectin⁃3;
autophagy;
AMPK/mTOR signaling pathway
- From:
Acta Universitatis Medicinalis Anhui
2023;58(9):1467-1473
- CountryChina
- Language:Chinese
-
Abstract:
Objective :To investigate the effects of D ⁃allose on the restoration of neurological function , Galectin⁃3 (Gal⁃3) , adenosine monophosphate⁃activated protein kinase/mammalian target of rapamycin (AMPK/mTOR) and the expression of some inflammatory factors in ischemia⁃reperfusion injury ( CIRI) mice .
Methods :A total of 50 male mice were randomly divided into control group (Con group) , sham group (Sham group) , cerebral ischemia⁃reperfusion injury group (MCAO group) , cerebral ischemia⁃reperfusion injury + D ⁃alolose group (MCAO + D ⁃allose group) and cerebral ischemia⁃reperfusion injury + modified citrus pectin group (MCAO + MCP group) . The middle cerebral artery occlusion/reperfusion (MCAO/R) model (reperfusion after 2 hours of MCA ischemia) was established by thread embolism . After successful modeling , the neurological function of mice was evaluated Longa score and rotated rod walking . TTC staining was used to observe the volume of cerebral infarction foci . The expression levels of Gal⁃3 and autophagy⁃related molecules were detected by Western blot and RT⁃PCR . Immunofluorescence was applied to detect the distribution of Gal⁃3 in brain tissue , and TNF⁃α , IL⁃8 secretion was detected with ELISA KIT .
Results :Compared with Con group and Sham group , the MCAO model represented significant increase in the
Longa neurofunction score (P < 0. 01) , cerebral infarction volume ( P < 0. 01) , Gal⁃3 expression and manifasted enhanced autophagy (P < 0. 01) . After treatment with D ⁃allose , it could significantly improve neurological dysfunction , reduce cerebral infarction volume (P < 0. 01) , reduce the expression of Gal⁃3 ( P < 0. 01) , inhibit AMPK phosphorylation , promote mTOR phosphorylation , and inhibit autophagy (P < 0. 01) . The use of the Gal⁃3 inhibitor MCP alone could also achieve the effect of inhibiting autophagy .
Conclusion : D ⁃allose can effectively promote the recovery of neurological function and reduce the volume of infarct foci in CIRI mice . The mechanism may involve inhibiting excessive cell autophagy by downregulating the expression of Gal⁃3 , and reducing the release of inflammatory factors such as TNF⁃α and IL⁃8 , thereby exerting neuroprotective effects .
- Full text:2024071617573854573D-阿洛糖下调半乳糖凝集素...R通路减轻脑缺血再灌注损伤_罗耀文.pdf
