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小檗碱通过干扰氧化应激和炎症通路来保护心脏免受缺血再灌注损伤。

Berberine Protests the Heart from Ischemic Reperfusion Injury via Interference with Oxidative and Inflammatory Pathways.

机构信息

Al-Sadar Teaching Medical City, Al-Najaf Open Heart and Interventional Cardiac Center. Najaf, Iraq.

College of Pharmacy, the Islamic University, 54001 Najaf, Iraq.

出版信息

Med Arch. 2021 Jun;75(3):174-179. doi: 10.5455/medarh.2021.75.174-179.

DOI:10.5455/medarh.2021.75.174-179
PMID:34483445
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8385727/
Abstract

BACKGROUND

Ischemia and reperfusion (I/R) is a pathological condition characterized by an initial restriction of blood supply to an organ followed by the subsequent restoration of perfusion and concomitant reoxygenation.

OBJECTIVE

The aim of the study is to assess the possible cardioprotective potential effect of berberine in myocardial ischemia reperfusion injury induced by ligation of coronary artery in a male rat model.

METHODS

Total amount of 28 adult male albino rats were randomized into 4 equal groups: 1) Sham group, rats underwent the same anesthetic and surgical procedure as the control group except for LAD ligation; 2), Active control group, rats subjected to regional ischemia for 30 min by ligation of LAD coronary artery and reperfusion for 2 hours, 3), Control vehicle group, rats received dimethyl sulphoxide (DMSO) (vehicle of berberine) via IP route and subjected to ischemia for 30 minutes before ligation of LAD coronary artery & reperfusion for 2 hr; 4), Berberine treated group, rats pretreated with berberine10 mg/kg via IP injection 30minutes before ligation of LAD coronary artery & then subjected to reperfusion for 2 hr.

RESULTS

In the control group, as compared with sham, tissue TNF-α, IL-6, IL-10, caspase-3 and BAX, plasma cTn-T and serum MDA significantly increased (P<0.05), while serum GSH significantly decreased (P<0.05). The histopathological control group showed a significant cardiac injury (P<0.05) compared with the sham group. Berberine significantly counteracted (P<0.05) the increase of TNF-α, IL-6, caspase-3 and BAX and counteracted the increase in plasma cTn-T and serum MDA. Berberine produces a significant elevation (P<0.05) in cardiac IL-10 and serum GSH with a significant reduction in (P<0.05) cardiac injury.

CONCLUSION

Berberine attenuates myocardial I/R injury in male rats via interfering with inflammatory reactions and apoptosis which were induced by I/R injury.

摘要

背景

缺血再灌注(I/R)是一种以器官初始血供受限为特征的病理状态,随后恢复灌注和伴随的再氧合。

目的

本研究旨在评估小檗碱在雄性大鼠冠状动脉结扎诱导的心肌缺血再灌注损伤中的可能心脏保护作用。

方法

总共 28 只成年雄性白化大鼠随机分为 4 组:1)假手术组,大鼠接受与对照组相同的麻醉和手术程序,但不结扎左前降支(LAD);2)活性对照组,大鼠通过结扎 LAD 冠状动脉缺血 30 分钟,再灌注 2 小时;3)对照组,大鼠通过腹腔注射二甲基亚砜(DMSO)(小檗碱的载体),然后结扎 LAD 冠状动脉前缺血 30 分钟,再灌注 2 小时;4)小檗碱治疗组,大鼠通过腹腔注射小檗碱 10mg/kg 预处理 30 分钟,然后结扎 LAD 冠状动脉,再灌注 2 小时。

结果

与假手术组相比,对照组的组织 TNF-α、IL-6、IL-10、caspase-3 和 BAX、血浆 cTn-T 和血清 MDA 明显升高(P<0.05),而血清 GSH 明显降低(P<0.05)。与假手术组相比,对照组的组织病理学显示出明显的心脏损伤(P<0.05)。小檗碱显著拮抗(P<0.05)TNF-α、IL-6、caspase-3 和 BAX 的增加,并拮抗血浆 cTn-T 和血清 MDA 的增加。小檗碱显著升高(P<0.05)心脏 IL-10 和血清 GSH,并显著降低(P<0.05)心脏损伤。

结论

小檗碱通过干扰 I/R 损伤诱导的炎症反应和细胞凋亡来减轻雄性大鼠的心肌 I/R 损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/993d/8385727/cb88adf5c1e8/medarch-75-174-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/993d/8385727/07585c1315c2/medarch-75-174-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/993d/8385727/7c2ea4c5b9ed/medarch-75-174-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/993d/8385727/8e854542de29/medarch-75-174-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/993d/8385727/659d515b105c/medarch-75-174-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/993d/8385727/be156753fb75/medarch-75-174-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/993d/8385727/0e479990fcaf/medarch-75-174-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/993d/8385727/613ec38ea2e4/medarch-75-174-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/993d/8385727/cdfa4e92dcb9/medarch-75-174-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/993d/8385727/cb88adf5c1e8/medarch-75-174-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/993d/8385727/07585c1315c2/medarch-75-174-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/993d/8385727/7c2ea4c5b9ed/medarch-75-174-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/993d/8385727/8e854542de29/medarch-75-174-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/993d/8385727/659d515b105c/medarch-75-174-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/993d/8385727/be156753fb75/medarch-75-174-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/993d/8385727/0e479990fcaf/medarch-75-174-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/993d/8385727/613ec38ea2e4/medarch-75-174-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/993d/8385727/cdfa4e92dcb9/medarch-75-174-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/993d/8385727/cb88adf5c1e8/medarch-75-174-g009.jpg

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