The molecular mechanism study of Sulforaphane inhibiting neurocellular apoptosis in brain tissue of rats with acute carbon monoxide poisoning
10.3969/j.issn.1008-9691.2024.06.013
- VernacularTitle:莱菔硫烷抑制急性一氧化碳中毒大鼠脑组织神经细胞凋亡的分子机制研究
- Author:
Aochun YUE
1
;
Huiping SONG
;
Xudong ZHOU
;
Zhongliang JI
;
Wei HAN
;
Qin LI
Author Information
1. 深圳大学总医院急诊科,广东 深圳 518055;青岛大学医学部中西医结合中心,山东 青岛 266071
- Publication Type:Journal Article
- Keywords:
Sulforaphane;
Acute carbon monoxide poisoning;
Apoptosis;
Apoptosis-related protein
- From:
Chinese Journal of Integrated Traditional and Western Medicine in Intensive and Critical Care
2024;31(6):714-719
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of sulforaphane(SFN)on the expression of apoptosis-related proteins(caspase-3 and caspase-9),in brain tissue of rats with acute carbon monoxide poisoning(ACOP),and to explore the molecular mechanism underlying its intervention in ACOP-induced brain injury.Methods The healthy male Sprague-Dawley(SD)rats were randomly assigned to three groups:normal control(NC)group,ACOP group,and SFN group,with 36 rats in each group.An ACOP animal model was established by exposing the rats to carbon monoxide(CO)in a hyperbaric oxygen chamber,while the rats in the NC group were allowed to breathe fresh air.The SFN group received an intraperitoneal injection of SFN 20 mg/kg within 2 hours after poisoning,once daily,until euthanasia.The NC and ACOP groups were injected with an equivalent volume of saline.Rats from each group were sacrificed on days 1,3,and 7 of the intervention to collect brain tissue,hematoxylin-eosin(HE)staining was performed to assess pathological damage in the brain tissue;Nissl staining was used to examine neuronal pathological changes;Immunohistochemistry was employed to detect the positive expression of caspase-3 and caspase-9 in the cortical region of the brain.Western blotting and quantitative reverse transcription-polymerase chain reaction(qRT-PCR)were conducted to measure the protein and mRNA expression of caspase-3 and caspase-9 in the brain tissue.Results After CO poisoning,brain tissue damage in the ACOP group progressively worsened,with a gradual decrease in the number of Nissl bodies and a gradual increase in the number of positive cells for caspase-3 and caspase-9 in the cortical region of the brain.The protein and mRNA expression of caspase-3 and caspase-9 in the brain tissue also gradually increased.Compared with the NC group at the same time point,the differences were statistically significant[Nissl bodies:69.33±0.94 vs.91.33±1.25;caspase-3 positive expression(A value):0.149±0.003 vs.0.113±0.004;caspase-9 positive expression(A value):0.178±0.002 vs.0.111±0.010;caspase-3 protein(caspase-3/GAPDH):1.634±0.045 vs.0.844±0.021;caspase-9 protein(caspase-9/GAPDH):1.754±0.024 vs.0.811±0.053;caspase-3 mRNA(2-ΔΔCt):1.718±0.052 vs.1;caspase-9 mRNA(2-ΔΔCt):1.722±0.066 vs.1,all P<0.05).Compared with the ACOP group at the same time point,the brain tissue damage in the SFN group improved,with a significant increase in the number of Nissl bodies(84.67±1.53 vs.69.33±0.94,P<0.05).The number of positive cells for caspase-3 and caspase-9 in the cortical region of the brain decreased significantly(A value:0.126±0.002 vs.0.149±0.003,0.127±0.002 vs.0.178±0.002,both P<0.05).The protein and mRNA expression of caspase-3 and caspase-9 in the brain tissue were significantly reduced[caspase-3 protein(caspase-3/GAPDH):0.999±0.037 vs.1.634±0.045;caspase-9 protein(caspase-9/GAPDH):0.993±0.040 vs.1.754±0.024;caspase-3 mRNA(2-ΔΔCt):1.120±0.059 vs.1.718±0.052;caspase-9 mRNA(2-ΔΔCt):0.520±0.045 vs.1.722±0.066,all P<0.05].Conclusion SFN partially attenuated ACOP-induced brain injury in rats,potentially by downregulating both protein and mRNA expression of caspase-3 and caspase-9,thereby reducing cellular apoptosis.
