Citri Reticulatae Pericarpium protects against isoproterenol-induced chronic heart failure via activation of PPARγ

Cheng, Hui‐Ling; Wu, Xiaodong; Ni, Gehui; Wang, Siqi; Peng, Wenjing; Zhang, Haifeng; Gao, Juan; Li, Xinli

doi:10.21037/atm-20-2200

Cited by 21 publications

(25 citation statements)

References 44 publications

(54 reference statements)

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“…It is characterized by impairment of cardiac systolic and diastolic functions, as well as irreversible cardiac dysfunction [1]. HF is a common end-phase of several cardiovascular diseases including hypertension, acute myocardial infarction, septic cardiomyopathy, and diabetic cardiomyopathy [2][3][4][5][6]. Alleviating cardiac dysfunction markedly prolongs the survival of patients with HF.…”

Section: Introductionmentioning

confidence: 99%

Lycorine ameliorates isoproterenol-induced cardiac dysfunction mainly via inhibiting inflammation, fibrosis, oxidative stress and apoptosis

Jiang

et al. 2021

Bioengineered

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Alleviating cardiac dysfunction improves the prognosis of heart failure patients. Lycorine is an alkaloid with several beneficial biological properties. Here, we used mice to evaluate the effect of lycorine on cardiac dysfunction elicited by isoproterenol. Mice were divided into four groups: control, lycorine, isoproterenol, and isoproterenol + lycorine. Mice in the combined group were treated daily with 10 mg/ kg isoproterenol intraperitoneally for 2 weeks and 5 mg/kg lycorine was given simultaneously intraperitoneally for 4 weeks. Cardiac structure and function were assessed by echocardiography, hematoxylin and eosin staining, and Masson's trichrome staining. Isoproterenol-induced cardiac dysfunction and histopathological injury that was significantly improved by treatment with lycorine. Western blotting and the quantitative real-time polymerase chain reaction were used to explore the molecular mechanisms of these effects. Levels of the inflammatory cytokines, interleukin (IL)-1β, IL-6, and tumor necrosis factor-α, were increased by treatment with isoproterenol; these increases were significantly reduced by lycorine, with involvement of the NF-κB signaling pathway. The fibrotic factors, collagen I and collagen III, were increased by isoproterenol and decreased by treatment with lycorine through inhibiting activation of the Smad signaling pathway. In addition, lycorine alleviated oxidative stress as evidenced by a reduction in total reactive oxygen species in the isoproterenol + lycorine group compared to the isoproterenol group. Lycorine exerted an anti-apoptotic effect as evidenced by upregulating Bcl-2 and downregulating Bax. Overall, our findings demonstrate that lycorine protects against cardiac dysfunction induced by isoproterenol by inhibiting inflammation, fibrosis, oxidative stress, and apoptosis.

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Section: Introductionmentioning

confidence: 99%

Lycorine ameliorates isoproterenol-induced cardiac dysfunction mainly via inhibiting inflammation, fibrosis, oxidative stress and apoptosis

Jiang

et al. 2021

Bioengineered

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“…Studies examining the effects of the traditional Chinese medicine qiliqiangxin capsule have revealed cardiac-protective functions mediated via PPAR γ regulation [ 8 ]. Citri reticulatae Pericarpium (CRP), a component of the qiliqiangxin capsule, inhibits pathological cardiac hypertrophy caused by multiple factors [ 9 , 10 ]. Nobiletin (NOB) is the active monomer isolated from CRP, with the molecular formula C 21 H 22 O 8 (the chemical structure is shown in Figure 1(a) ).…”

Section: Introductionmentioning

confidence: 99%

Nobiletin Attenuates Pathological Cardiac Remodeling after Myocardial Infarction via Activating PPARγ and PGC1α

et al. 2021

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Rationale. Pathological cardiac remodeling serves as a vital mechanism during the progression from myocardial infarction (MI) to chronic heart failure (CHF). Nobiletin (NOB), an active monomer extracted from the peel of citrus fruit, has been reported to have beneficial effects in cardiovascular diseases. Our study was aimed at describing the specific mechanisms through which NOB protects against pathological cardiac remodeling after MI. Materials and Methods. C57BL/6 mice were treated with coronary artery ligation to generate an MI model, followed by treatment for 3 weeks with NOB (50 mg/kg/d) or vehicle (50 mg/kg/d), with or without the peroxisome proliferator-activated receptor gamma (PPARγ) inhibitor T0070907 (1 mg/kg/d). Cardiac function (echocardiography, survival rate, Evans blue, and triphenyl tetrazolium chloride staining), fibrosis (Masson’s trichrome staining, quantitative real-time polymerase chain reaction (qRT-PCR), and western blot (WB)), hypertrophy (haematoxylin-eosin staining, wheat germ agglutinin staining, and qRT-PCR), and apoptosis (WB and terminal deoxynucleotidyl transferase dUTP nick-end labelling (TUNEL) staining) were evaluated. Hypoxia-induced apoptosis (TUNEL, WB) and phenylephrine- (PE-) induced pathological hypertrophy (immunofluorescence staining, qRT-PCR) models were established in primary neonatal rat ventricular myocytes (NRVMs). The effects of NOB with or without T0070907 were examined for the expression of PPARγ and PPARγ coactivator 1α (PGC1α) by WB in mice and NRVMs. The potential downstream effectors of PPARγ were further analyzed by WB in mice. Results. Following MI in mice, NOB intervention enhanced cardiac function across three predominant dimensions of pathological cardiac remodeling, which reflected in decreasing cardiac fibrosis, apoptosis, and hypertrophy decompensation. NOB intervention also alleviated apoptosis and hypertrophy in NRVMs. NOB intervention upregulated PPARγ and PGC1α in vivo and in vitro. Furthermore, the PPARγ inhibitor abolished the protective effects of NOB against pathological cardiac remodeling during the progression from MI to CHF. The potential downstream effectors of PPARγ were nuclear factor erythroid 2-related factor 2 (Nrf-2) and heme oxygenase 1 (HO-1). Conclusions. Our findings suggested that NOB alleviates pathological cardiac remodeling after MI via PPARγ and PGC1α upregulation.

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“…in the current study, to obtain more evidence to further transform the application of Sch a in clinical patient management, mice were used to construct cHF models for in vivo and nrVMs isolated from rat pups for in vitro. rat and mouse experiments are involved in the previous studies and, by contrast, the mouse cHF model is more mature, while the rat cell extraction is easier (30)(31)(32). The present study demonstrated the protective effects of Sch a in cHF via the administration of Sch a.…”

Section: Discussionmentioning

confidence: 99%

Schisandrin A protects against isoproterenol‑induced chronic heart failure via miR‑155

Gao

et al. 2021

Mol Med Rep

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Citri Reticulatae Pericarpium protects against isoproterenol-induced chronic heart failure via activation of PPARγ

Cited by 21 publications

References 44 publications

Lycorine ameliorates isoproterenol-induced cardiac dysfunction mainly via inhibiting inflammation, fibrosis, oxidative stress and apoptosis

Lycorine ameliorates isoproterenol-induced cardiac dysfunction mainly via inhibiting inflammation, fibrosis, oxidative stress and apoptosis

Nobiletin Attenuates Pathological Cardiac Remodeling after Myocardial Infarction via Activating PPARγ and PGC1α

Schisandrin A protects against isoproterenol‑induced chronic heart failure via miR‑155

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