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

doi:https://doi.org/10.1016/j.chmed.2023.11.001

Archive > Volume 16 Issue 2 > 2024,16(2):282-292. DOI:https://doi.org/10.1016/j.chmed.2023.11.001 Prev Next

銀杏葉通過提高Bcl-2/mTOR/ERK1/2/Na+，K+- ATP酶活性對異丙腎上腺素所致心肌梗死的多效減弱作用

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

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摘要:

目的：心肌梗死(MI)與心肌血氧供需失衡有關(guān)。受體阻滯劑和鈣拮抗劑只是治療心肌梗死的兩種常用藥物。然而，據(jù)報(bào)道，這些藥物要么無效，要么有不良副作用。銀杏葉提取物(GBE)，一種中草藥產(chǎn)品，在炎癥性疾病和氧化應(yīng)激的治療中提供特殊的相容性益處。為了更好地了解GBE對異丙腎上腺素(ISO)損傷大鼠心肌梗死的影響，設(shè)計(jì)了本研究。方法：心臟重量指數(shù)、血脂譜、心臟標(biāo)記酶、內(nèi)源性抗氧化劑[過氧化氫酶(CAT)、超氧化物歧化酶(SOD)、谷胱甘肽(GSH)、亞硝酸鹽和丙二醛(MDA)]、炎癥介質(zhì)[腫瘤壞死因子α (TNF-α)和白細(xì)胞介素6 (IL-6)]、b細(xì)胞淋巴瘤因子-2 (Bcl-2)、細(xì)胞外信號(hào)調(diào)節(jié)激酶(ERK1/2)的免疫組織化學(xué)表達(dá)、和哺乳動(dòng)物雷帕霉素靶蛋白(mTOR)和組織病理學(xué)分析來評估GBE的心臟保護(hù)特性。結(jié)果：GBE通過增強(qiáng)機(jī)體天然抗氧化防御系統(tǒng)，減少炎癥細(xì)胞因子和心臟損傷標(biāo)志酶的釋放，有效減輕心肌梗死。Bcl-2、ERK1/2、mTOR表達(dá)增加，組織形態(tài)學(xué)改變逆轉(zhuǎn)。結(jié)論：GBE的心臟保護(hù)作用可能與Bcl-2/ mTOR/ERK1/2/Na+，K+- ATP酶活性增加有關(guān)。

Abstract:

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 MI. However, these have reportedly been shown to be either ineffective or to have undesirable side effects. Extract of Ginkgo biloba leaves (GBE), a Chinese herbal product offers special compatibility 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)], immunohistochemical 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 histomorphological 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.

關(guān)鍵詞:

抗氧化劑;細(xì)胞外信號(hào)調(diào)節(jié)激酶;銀杏葉提取物;異丙腎上腺素;哺乳動(dòng)物雷帕霉素靶點(diǎn);心肌梗死;Na+，K+- ATP酶

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