The cardioprotective and anxiolytic effects of Chaihujialonggumuli granule on rats with anxiety after acute myocardial infarction is partly mediated by suppression of CXCR4/NF-κB/GSDMD pathway

Hou, Jiqiu; Wang, Chao; Ma, Di; Chen, Yali; Jin, Huihui; An, Ying; Jia, Jingyun; Huang, Lexi; Zhao, Haibin

doi:10.1016/j.biopha.2020.111015

Cited by 25 publications

(13 citation statements)

References 54 publications

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“…NF-κB is a family of transcription factors that controls many cellular processes in disease, such as inflammation, proliferation, as well as angiogenesis. A recent study has shown that blocking NF-κB could protect the heart against inflammatory responses and acute ischemic injury (Hou et al, 2021). Previous studies have elucidated that AS-IV could inhibit high glucose-induced NLRP3 inflammasome activation and subsequent secretion of pro-inflammatory cytokines via inhibiting TLR4/NF-κB signaling pathway and CaSR, which provides new insights into the anti-inflammatory activity of AS-IV (Leng et al, 2019).…”

Section: Discussionmentioning

confidence: 97%

Astragaloside IV promotes cardiac remodeling after myocardial infarction by inhibiting DNMT3B-mediated Runx3 methylation via downregulating LncRNA MIRT1 expression

et al. 2022

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Astragaloside IV (AS-IV) has been shown to possess cardioprotective effect. However, the specific mechanism of AS-IV in myocardial infarction (MI) remains unclear. Our results showed that AS-IV intervention observably enhanced cell viability and reduced cell apoptosis, oxidative stress levels and inflammatory factor secretion. Expression of MIRT1 was significantly up-regulated in hypoxia-treated cells. In addition, ALCAM overexpression reversed the effects of AS-IV intervention on hypoxia-treated cell functions. MIRT1 facilitated Runx3 promoter methylation and its downregulated expression by recruiting DNA methyltransferase 3B (DNMT3B) to the Runx3 promoter region through binding with suppressor of Zeste 12 protein homolog (Suz12). Runx3 silencing reversed the effects of MIRT1 inhibition on hypoxia-treated cell functions. Betulinic acid suppressed the effects of AS-IV intervention on the behaviors of hypoxia-treated cells. AS-IV treatment improved the cardiac functions of mice with MI. Taken together, these findings demonstrated that AS-IV treatment inhibits DNMT3B-mediated Runx3 promoter methylation by restraining Suz12 expression and further blocks the NF-κB signaling pathway, and in turn improves the cardiac functions of mice with MI.

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Section: Discussionmentioning

confidence: 97%

Astragaloside IV promotes cardiac remodeling after myocardial infarction by inhibiting DNMT3B-mediated Runx3 methylation via downregulating LncRNA MIRT1 expression

et al. 2022

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“…Recently, Shi et al found that GSDMD and GSDMD-N were significantly increased in mouse heart tissue and human peripheral blood samples of I/R, and knockout of GSDMD could reduce myocardial injury [20]. Hou et al found that the level of GSDMD was significantly upregulated in the myocardial tissue of the AMI rat model [37], while Ye et al reported that the level of GSDMD-N was significantly increased in I/R rats [38]. Lei et al reported that the level of GSDMD and active subunit GSDMD-N in H9C2 cells significantly increased after oxygen-glucose deprivation [39].…”

Section: Discussionmentioning

confidence: 99%

Inhibition of GSDMD Activates Poly(ADP-ribosyl)ation and Promotes Myocardial Ischemia-Reperfusion Injury

Zhang

Chen

et al. 2022

Oxidative Medicine and Cellular Longevity

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The precise control of cardiomyocyte viability is imperative to combat myocardial ischemia-reperfusion injury (I/R), in which apoptosis and pyroptosis putatively contribute to the process. Recent researches indicated that GSDMD is involved in I/R as an executive protein of pyroptosis. However, its effect on other forms of cell death is unclear. We identified that GSDMD and GSDMD-N levels were significantly upregulated in the I/R myocardium of mice. Knockout of GSDMD conferred the resistance of the hearts to reperfusion injury in the acute phase of I/R but aggravated reperfusion injury in the chronic phase of I/R. Mechanistically, GSDMD deficiency induced the activation of PARylation and the consumption of NAD+ and ATP, leading to cardiomyocyte apoptosis. Moreover, PJ34, a putative PARP-1 inhibitor, reduced the myocardial injury caused by GSDMD deficiency. Our results reveal a novel action modality of GSDMD in the regulation of cardiomyocyte death; inhibition of GSDMD activates PARylation, suggesting the multidirectional role of GSDMD in I/R and providing a new theory for clinical treatment.

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“…Acute myocardial infarction (AMI) is characterized by sudden onset, rapid advancement and high mortality. Therefore, patients should be sent to hospital for emergency treatment as soon as they show signs of AMI [17][18][19]. One of the most frequently used methods for the treatment of myocardial infarction is PCI.…”

Section: Discussionmentioning

confidence: 99%

Combined administration of nicorandil and atorvastatin in patients with acute myocardial infarction after coronary intervention, and its effect on postoperative cardiac systolic function

Sun¹,

Zhang²,

Shen³

2021

Trop. J. Pharm Res

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Purpose: To study the effect of a combination of nicorandil and atorvastatin calcium in patients with acute myocardial infarction after coronary intervention, and its effect on postoperative cardiac systolic function of patients.Methods: Retrospective analysis was performed on 100 patients with acute myocardial infarctiontreated with coronary interventional therapy in The Third Affiliated Hospital of Qiqihaer MedicalUniversity from April 2019 to August 2020. The patients were randomised into control and study groups, with 50 patients in each group. The control group was treated with nicorandil, while the study group was treated with a combination of nicorandil and atorvastatin. Treatment response, cardiac structural indices, cardiac systolic function, blood lipid profiles, quality of life (QLI) score, Barthel Index (BI), Fugl- Meyer assessment (FMA), motor function score, incidence of adverse reactions, and blood pressure changes on days 1, 2, 3 and 4 after surgery, were compared between the two groups.Results: Treatment effectiveness, cardiac systolic function, QLI score, BI index and FMA motor function score in the study group were higher than the corresponding control values (p < 0.05). However, lower cardiac structure indices, blood lipid profiles and incidence of adverse reactions were greater in the study group than in the control group (p < 0.05). No significant disparity in blood pressure was found between the two groups on post-surgery days 1, 2, 3 and 4.Conclusion: The combination of nicorandil and atorvastatin calcium tablets produced better outcomes in patients with acute myocardial infarction after coronary intervention therapy; furthermore, the combination therapy significantly improved the cardiac systolic function of patients.

show abstract

The cardioprotective and anxiolytic effects of Chaihujialonggumuli granule on rats with anxiety after acute myocardial infarction is partly mediated by suppression of CXCR4/NF-κB/GSDMD pathway

Cited by 25 publications

References 54 publications

Astragaloside IV promotes cardiac remodeling after myocardial infarction by inhibiting DNMT3B-mediated Runx3 methylation via downregulating LncRNA MIRT1 expression

Astragaloside IV promotes cardiac remodeling after myocardial infarction by inhibiting DNMT3B-mediated Runx3 methylation via downregulating LncRNA MIRT1 expression

Inhibition of GSDMD Activates Poly(ADP-ribosyl)ation and Promotes Myocardial Ischemia-Reperfusion Injury

Combined administration of nicorandil and atorvastatin in patients with acute myocardial infarction after coronary intervention, and its effect on postoperative cardiac systolic function

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