首页|Pleiotropic attenuating effect of Ginkgo biloba against isoprenaline-induced myocardial infarction via improving Bcl-2/mTOR/ERK1/2/Na+,K+-ATPase activities

Pleiotropic attenuating effect of Ginkgo biloba against isoprenaline-induced myocardial infarction via improving Bcl-2/mTOR/ERK1/2/Na+,K+-ATPase activities

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Objective:Myocardial infarction(MI)is linked to an imbalance in the supply and demand of blood oxygen in the heart muscles.Beta-blockers and calcium antagonists are just two of the common medications used to treat Ml.However,these have reportedly been shown to be either ineffective or to have undesir-able side effects.Extract of Ginkgo biloba leaves(GBE),a Chinese herbal product offers special compati-bility benefits in therapeutic settings relating to inflammatory diseases and oxidative stress.In order to better understand how GBE affects MI in rats insulted by isoprenaline(ISO),the current study was designed.Methods:The heart weight index,serum lipid profile,cardiac marker enzymes,endogenous antioxidants[catalase(CAT),superoxide dismutase(SOD),glutathione(GSH),nitrites and malondialdehyde(MDA)],inflammatory mediators[tumour necrosis factor alpha(TNF-α)and interleukin-6(IL-6)],immunohisto-chemical expressions of B-cell lymphoma factor-2(Bcl-2),extracellular signal-regulated kinase(ERK1/2),and mammalian target of rapamycin(mTOR)and histopathological analysis were used to assess the cardioprotective properties of GBE.Results:The findings showed that GBE effectively attenuated myocardial infarction by boosting the body's natural antioxidant defense system and reducing the release of inflammatory cytokines as well as heart injury marker enzymes.The expression of Bcl-2,ERK1/2 and mTOR was increased while the his-tomorphological alterations were reversed.Conclusion:The cardioprotective effects of GBE may be due to a mechanism involving increased Bcl-2/mTOR/ERK1/2/Na+,K+-ATPase activity.

antioxidantsextracellular signal-regulated kinaseGinkgo biloba extractisoprenalinemammalian target of rapamycinmyocardial infarctionNa+,K+-ATPase

Jerome Ndudi Asiwe、Abodunrin Adebayo Ojetola、Nwoke Enekabokom Ekene、Esthinsheen Osirim、Anthony Chibuzor Nnamudi、Benjamin Oritsemuelebi、Jackson Erozueme Onuelu、Nicholas Asiwe、Harrison Ogheneochuko Eruotor、Saviour Inegbenehi

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Department of Physiology,Delta State University,Abraka 1,Nigeria

Department of Physiology,University of Ibadan,Ibadan 3017,Nigeria

Department of Physiology,Adeleke University,Ede 250,Nigeria

Department of Pharmacology,Rivers State University,Nkpolu-Oroworukwo 5080,Nigeria

Department of Physiology,Redeemer's University,Ede 230,Nigeria

Department of Biochemistry,PAMO University of Medical Sciences,Port Harcourt 500211,Nigeria

Department of Pharmacology,Delta State University,Abraka 1,Nigeria

Department of Anatomy,University of Port Harcourt,Choba 5323,Nigeria

Department of Medical Laboratory Sciences,University of Port Harcourt,Choba 5323,Nigeria

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2024

10.1016/j.chmed.2023.11.001

中草药(英文版)
天津药物研究院 中国医学科学院药用植物研究所

中草药(英文版)

CSTPCD
影响因子：0.6
ISSN：1674-6384
年,卷(期)：2024.16(2)
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