摘要
目的 探讨氢气通过B淋巴细胞瘤/白血病-2相关X蛋白(Bax)/半胱氨酸天冬氨酸蛋白酶3(Caspase3)凋亡通路对大鼠创伤性脑损伤的改善作用。方法 56只SD大鼠分为对照组、模型组、氢气+通路激活组、氢气组,每组14只,制作创伤性脑损伤大鼠模型,造模结束后,氢气组每天吸入1 h氢气(42% H_(2)-21% O_(2)-37%N),氢气+通路激活组应用氢气+5μg Bax/Caspase3激活剂干预。干预7 d后,比较4组神经损伤严重程度评分(NSS)、脑含水率、脑组织病理形态变化、白细胞介素-1β(IL-1β)、肿瘤坏死因子-α(TNF-α)、超氧化物歧化酶(SOD)、丙二醛(MDA)及Bax/Caspase3通路蛋白表达量变化。结果 氢气组脑组织病理变化较模型组明显减轻,病灶区和水肿区缩小,变性坏死、出血坏死及炎性浸润减少;氢气+通路激活组对脑组织病理的改善作用较氢气组有所减弱。模型组NSS、脑含水率、TNF-α、IL-1β、MDA及Bax、Caspase3蛋白表达量高于对照组,SOD水平低于对照组(P<0.05);氢气组NSS、脑含水率、TNF-α、IL-1β、MDA及Bax、Caspase3蛋白表达量低于模型组和氢气+通路激活组,SOD水平高于模型组和氢气+通路激活组(P<0.05)。结论 氢气对大鼠创伤性脑损伤具有一定改善作用,能够降低大鼠炎症和氧化应激水平,减轻脑组织病理损伤,其机制可能与氢气抗Bax/Caspase3凋亡通路有关。
Objective To investigate the effect of hydrogen on attenuating traumatic brain injury(TBI) in rats through B-lymphoma/leukemia-2-related X-protein(Bax)/cysteine aspartate proteinase3(Caspase3) apoptosis pathway. Methods Fifty-six SD rats were divided into control group, model group, hydrogen + pathway activation group, and hydrogen group, with 14 rats in each group, a rat model of TBI was established. After successful modeling, the hydrogen group was given inhaled hydrogen(42% H_(2)-21% O_(2)-37% N) for 1 h every day, and the hydrogen+pathway activation group was intervened with hydrogen+5 μg Bax/Caspase3 activator. At 7 d after intervention, the neurological severity score(NSS), brain water content, histopathological changes in brain tissue, and changes in interleukin-1β(IL-1β), tumor necrosis factor-α(TNF-α), the expression of superoxide dismutase(SOD), malondialdehyde(MDA) and Bax/Caspase3 pathway proteins were compared among the four groups. Results Compared with the model group, the pathological changes of the brain tissue in the hydrogen group were significantly smaller, the lesion area and edema area were reduced, and the degeneration and necrosis, hemorrhagic necrosis and inflammatory infiltration were reduced. Compared with the hydrogen group, the improvement effect of the hydrogen + pathway activation group on brain histopathology was weakened. The NSS score, brain water content, TNF-α, IL-1β, MDA and Bax, Caspase3 protein expressions in the model group were higher than those in the control group, while the SOD level was lower than that in the control group(P<0.05). The NSS score, brain water content, TNF-α, IL-1β, MDA and Bax, Caspase3 protein expression was lower in the hydrogen group than in the model group and hydrogen+pathway activation group, while SOD level was higher than that in the model group and hydrogen+pathway activation group(P<0.05). Conclusion Hydrogen can improve TBI in rats, reduce the level of inflammation and oxidative stress, and alleviate the pathological damage of brain tissue. The mechanism may be related to the anti-Bax/Caspase3 apoptosis pathway of hydrogen.
作者
钱波
冯莹
邹卓群
QIAN Bo;FENG Ying;ZOU Zhuo-qun(Department of Geriatrics,East China Nursing Home,Wuxi,Jiangsu 214000,China)
出处
《临床误诊误治》
CAS
2022年第7期102-106,共5页
Clinical Misdiagnosis & Mistherapy
基金
江苏省卫生计生委科研课题资助项目(H2018010756)。
