Ghrelin ameliorates cardiac fibrosis after myocardial infarction by regulating the Nrf2/NADPH/ROS pathway

Wang, Qian; Liu, Aidong; Li, Tianshu; Tang, Qian; Wang, Xiancheng; Chen, Xuebin

doi:10.1016/j.peptides.2021.170613

Cited by 12 publications

(9 citation statements)

References 41 publications

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“…Myocardial bleaching and ST-segment elevation on the electrocardiogram indicated that the model was successfully established. [27][28][29] The sham-operated group was operated on identically except that the coronary artery was not ligated. The animals were carefully monitored during the establishment of the model.…”

Section: Establishment Of MI Modelmentioning

confidence: 99%

Liquiritin Protects Against Cardiac Fibrosis After Myocardial Infarction by Inhibiting CCL5 Expression and the NF-κB Signaling Pathway

Han¹,

Yang²,

Li³

et al. 2022

DDDT

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Purpose Despite significant advances in interventional treatment, myocardial infarction (MI) and subsequent cardiac fibrosis remain major causes of high mortality worldwide. Liquiritin (LQ) is a flavonoid extract from licorice that possesses a variety of pharmacological properties. However, to our knowledge, the effects of LQ on myocardial fibrosis after MI have not been reported in detail. The aim of our research was to explore the potential role and mechanism of LQ in MI-induced myocardial damage. Methods The MI models were established by ligating the left anterior descending branch of the coronary artery. Next, rats were orally administered LQ once a day for 14 days. Biochemical assays, histopathological observations, ELISA, and Western blotting analyses were then conducted. Results LQ improved the heart appearance and ECG, decreased cardiac weight index and reduced levels of cardiac-specific markers such as CK, CK-MB, LDH, cTnI and BNP. Meanwhile, LQ reduced myocardial infarct size and improved hemodynamic parameters such as LVEDP, LVSP and ±dp/dt max . Moreover, H&E staining showed that LQ attenuated the pathological damage caused by MI. Masson staining showed that LQ alleviated myocardial cell disorder and fibrosis while reducing collagen deposition. LQ also decreased the levels of oxidative stress and inflammation. Western blotting demonstrated that LQ significantly down-regulated the expressions of Collagen I, Collagen III, TGF-β1, MMP-9, α-SMA, CCL5, and p-NF-κB. Conclusion LQ protected against myocardial fibrosis following MI by improving cardiac function, and attenuating oxidative damage and inflammatory response, which may be associated with inhibition of CCL5 expression and the NF-κB pathway.

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Section: Establishment Of MI Modelmentioning

confidence: 99%

Liquiritin Protects Against Cardiac Fibrosis After Myocardial Infarction by Inhibiting CCL5 Expression and the NF-κB Signaling Pathway

Han¹,

Yang²,

Li³

et al. 2022

DDDT

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“…Other studies also demonstrated that fullerol alleviates the inflammatory response by inhibiting ROS/p38MAPK/NF-κB and ROS/p38MAPK/FoxO1 pathways [ 81 ]. In the MIRI model of NADPH oxidase knockout mice, ROS production is reduced, and the myocardial infarction area is also reduced [ 82 ]. In the H9c2 cells injured by H/R, activation of the SIRT1/FOXO1/Mn-SOD antioxidant signaling pathway reduces H/R-induced ROS production, playing a protective role in cardiomyocytes [ 83 ].…”

Section: Discussionmentioning

confidence: 99%

Mechanism of Action of Flavonoids of Oxytropis falcata on the Alleviation of Myocardial Ischemia–Reperfusion Injury

et al. 2022

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Oxytropis falcata Bunge is a plant used in traditional Tibetan medicine, with reported anti-inflammatory and antioxidants effects and alleviation of myocardial ischemia reperfusion injury (MIRI). However, the underlying mechanism against MIRI and the phytochemical composition of O. falcata are vague. One fraction named OFF1 with anti-MIRI activity was obtained from O. falcata, and the chemical constituents were identified by ultra-high-performance liquid chromatography coupled with tandem mass spectrometry (UHPLC–MS). The potential targets and signaling pathways involved in the action of O. falcata against MIRI were predicted by network pharmacology analysis, and its molecular mechanism on MIRI was determined by in vitro assays. The results revealed that flavonoids are the dominant constituents of OFF1. A total of 92 flavonoids reported in O. falcata targeted 213 potential MIRI-associated factors, including tumor necrosis factor (TNF), prostaglandin-endoperoxide synthase 2 (PTGS2), and the NF-κB signaling pathway. The in vitro assay on H9c2 cardiomyocytes subjected to hypoxia/reoxygenation injury confirmed that the flavonoids in OFF1 reduced myocardial marker levels, apoptotic rate, and the inflammatory response triggered by oxidative stress. Moreover, OFF1 attenuated MIRI by downregulating the ROS-mediated JNK/p38MAPK/NF-κB pathway. Collectively, these findings provide novel insights into the molecular mechanism of O. falcata in alleviating MIRI, being a potential therapeutic candidate.

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“…Increasing evidence demonstrates that the renin-angiotensin-aldosterone system (RAAS) is activated in patients with MI [ 24 ]. Angiotensin II (Ang II) is an important active component RAS, playing an important role on myocardial oxidative stress, collagen formation, and impaired ejection fraction [ 25 , 26 ]. Ang II has also been shown to upregulate inflammation in a mouse model of MI [ 27 ].…”

Section: Discussionmentioning

confidence: 99%

Flavonoid Extract from Propolis Provides Cardioprotection following Myocardial Infarction by Activating PPAR-γ

Wang

Chen

Tang

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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We have previously reported that flavonoid extract from propolis (FP) can improve cardiac function in rats following myocardial infarction (MI). However, the mechanisms responsible for the cardioprotective effects of FP have not been fully elucidated. In the current study, we explored whether FP can reduce inflammatory cytokines and attenuate sympathetic nerve system activity and antiendoplasmic reticulum (ER) stress and whether the cardioprotective effects are related to peroxisome proliferator-activated receptor gamma (PPAR-γ) activation. Sprague Dawley rats were randomly divided into six groups: Sham group received the surgical procedure but no artery was ligated; MI group received ligation of the left anterior descending (LAD) branch of the coronary artery; MI + FP group received FP (12.5 mg/kg/d, intragastrically) seven days prior to LAD ligation; FP group (Sham group + 12.5 mg/kg/d, intragastrically); MI + FP + GW9662 group received FP prior to LAD ligation with the addition of a specific PPAR-γ inhibitor (GW9662), 1 mg/kg/d, orally); and MI + GW9662 group received the PPAR-γ inhibitor and LAD ligation. The results demonstrated that the following inflammatory markers were significantly elevated following MI as compared with expression in sham animals: IL-1β, TNF-α, CRP; markers of sympathetic activation: plasma norepinephrine, epinephrine and GAP43, nerve growth factor, thyroid hormone; and ER stress response markers GRP78 and CHOP. Notably, the above changes were attenuated by FP, and GW9662 was able to alleviate the effect of FP. In conclusion, FP induces a cardioprotective effect following myocardial infarction by activating PPAR-γ, leading to less inflammation, cardiac sympathetic activity, and ER stress.

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Ghrelin ameliorates cardiac fibrosis after myocardial infarction by regulating the Nrf2/NADPH/ROS pathway

Cited by 12 publications

References 41 publications

Liquiritin Protects Against Cardiac Fibrosis After Myocardial Infarction by Inhibiting CCL5 Expression and the NF-κB Signaling Pathway

Liquiritin Protects Against Cardiac Fibrosis After Myocardial Infarction by Inhibiting CCL5 Expression and the NF-κB Signaling Pathway

Mechanism of Action of Flavonoids of Oxytropis falcata on the Alleviation of Myocardial Ischemia–Reperfusion Injury

Flavonoid Extract from Propolis Provides Cardioprotection following Myocardial Infarction by Activating PPAR-γ

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