Polydatin improves intestinal barrier injury after traumatic brain injury in rats by reducing oxidative stress and inflammatory response via activating SIRT1-mediated deacetylation of SOD2 and HMGB1 / 南方医科大学学报
Journal of Southern Medical University
; (12): 93-100, 2022.
Article
in Zh
| WPRIM
| ID: wpr-936289
Responsible library:
WPRO
ABSTRACT
OBJECTIVE@#To investigate the protective effect against intestinal mucosal injury in rats following traumatic brain injury (TBI) and explore the underlying mechanism.@*METHODS@#SD rat models of TBI were established by fluid percussion injury (FPI), and the specimens were collected at 12, 24, 48, and 72 h after TBI. Another 15 rats were randomly divided into shamoperated group (n=5), TBI with saline treatment (TBI+NS) group (n=5), and TBI with PD treatment (TBI+PD) group (treated with 30 mg/kg PD after TBI; n=5). Body weight gain and fecal water content of the rats were recorded, and after the treatments, the histopathology of the jejunum was observed, and the levels of D-lactic acid (D-LAC), diamine oxidase (DAO), ZO-1, claudin-5, and reactive oxygen species (ROS) were detected. Lipid peroxide (LPO) and superoxide dismutase (SOD) 2 content, jejunal pro-inflammatory factors (IL-6, IL-1β, and TNF- α), Sirt1 activity, SOD2 and HMGB1 acetylation level were also determined after the treatments.@*RESULTS@#The rats showed significantly decreased body weight and fecal water content and progressively increased serum levels of D-LAC and DAO after TBI (P < 0.05) with obvious jejunal injury, significantly decreased expression levels of ZO-1 and claudin-5, lowered SOD2 and Sirt1 activity (P < 0.05), increased expression levels of LPO, ROS, and pro-inflammatory cytokines, and enhanced SOD2 and HMGB1 acetylation levels (P < 0.05). Compared with TBI+NS group, the rats in TBI+PD group showed obvious body weight regain, increased fecal water content, reduced jejunal pathologies, decreased D-LAC and DAO levels (P < 0.05), increased ZO-1, claudin-5, SOD2 expression levels and Sirt1 activity, and significantly decreased ROS, LPO, pro-inflammatory cytokines, and acetylation levels of SOD2 and HMGB1 (P < 0.05).@*CONCLUSION@#PD alleviates oxidative stress and inflammatory response by activating Sirt1-mediated deacetylation of SOD2 and HMGB1 to improve intestinal mucosal injury in TBI rats.
Key words
Full text:
1
Index:
WPRIM
Main subject:
Stilbenes
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Superoxide Dismutase
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Rats, Sprague-Dawley
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Oxidative Stress
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HMGB1 Protein
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Sirtuin 1
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Brain Injuries, Traumatic
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Glucosides
Type of study:
Prognostic_studies
Limits:
Animals
Language:
Zh
Journal:
Journal of Southern Medical University
Year:
2022
Type:
Article