Sodium Houttuyfonate Alleviates Post-infarct Remodeling in Rats via AMP-Activated Protein Kinase Pathway

Cheng, Zheng; Lin, Jiafeng; Lin, Zhonghao; Lin, Wei-Qian; Thapa, Saroj; Lin, Yuan‐Zheng; Lian, Hao; Liu, Zhi-Rui; Chen, Jiahui; Li, Xiaowei

doi:10.3389/fphar.2018.01092

Cited by 16 publications

(7 citation statements)

References 25 publications

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“…The cardiac characteristics observed in this study are consistent with previous reports using this model of HF [41][42][43]. Additionally, substantial number of previous studies [44][45][46][47][48][49][50][51] demonstrated that natriuretic peptide levels in both the heart and the serum are significantly increased in rats with HF induced by coronary artery ligation used in the current study. Taken together, the ˃ 30% infarct size, increased LVEDP, LVEDD, LVESD, LVEDV and LVESV and decreased dP/dt, FS, EF, SV and CO all indicate that rats in HF group were experiencing cardiac dysfunction.…”

Section: Cardiac Characteristics Of the Hf Modelsupporting

confidence: 92%

GLP-1 mediated diuresis and natriuresis are blunted in heart failure and restored by selective afferent renal denervation

Katsurada

Nandi

Zheng

et al. 2020

Cardiovasc Diabetol

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Background: Glucagon-like peptide-1 (GLP-1) induces diuresis and natriuresis. Previously we have shown that GLP-1 activates afferent renal nerve to increase efferent renal sympathetic nerve activity that negates the diuresis and natriuresis as a negative feedback mechanism in normal rats. However, renal effects of GLP-1 in heart failure (HF) has not been elucidated. The present study was designed to assess GLP-1-induced diuresis and natriuresis in rats with HF and its interactions with renal nerve activity. Methods: HF was induced in rats by coronary artery ligation. The direct recording of afferent renal nerve activity (ARNA) with intrapelvic injection of GLP-1 and total renal sympathetic nerve activity (RSNA) with intravenous infusion of GLP-1 were performed. GLP-1 receptor expression in renal pelvis, densely innervated by afferent renal nerve, was assessed by real-time PCR and western blot analysis. In separate group of rats after coronary artery ligation selective afferent renal denervation (A-RDN) was performed by periaxonal application of capsaicin, then intravenous infusion of GLP-1-induced diuresis and natriuresis were evaluated. Results: In HF, compared to sham-operated control; (1) response of increase in ARNA to intrapelvic injection of GLP-1 was enhanced (3.7 ± 0.4 vs. 2.0 ± 0.4 µV s), (2) GLP-1 receptor expression was increased in renal pelvis, (3) response of increase in RSNA to intravenous infusion of GLP-1 was enhanced (132 ± 30% vs. 70 ± 16% of the baseline level), and (4) diuretic and natriuretic responses to intravenous infusion of GLP-1 were blunted (urine flow 53.4 ± 4.3 vs. 78.6 ± 4.4 µl/min/gkw, sodium excretion 7.4 ± 0.8 vs. 10.9 ± 1.0 µEq/min/gkw). A-RDN induced significant increases in diuretic and natriuretic responses to GLP-1 in HF (urine flow 96.0 ± 1.9 vs. 53.4 ± 4.3 µl/min/gkw, sodium excretion 13.6 ± 1.4 vs. 7.4 ± 0.8 µEq/min/gkw). Conclusions: The excessive activation of neural circuitry involving afferent and efferent renal nerves suppresses diuretic and natriuretic responses to GLP-1 in HF. These pathophysiological responses to GLP-1 might be involved in the interaction between incretin-based medicines and established HF condition. RDN restores diuretic and natriuretic effects of GLP-1 and thus has potential beneficial therapeutic implication for diabetic HF patients.

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Section: Cardiac Characteristics Of the Hf Modelsupporting

confidence: 92%

GLP-1 mediated diuresis and natriuresis are blunted in heart failure and restored by selective afferent renal denervation

Katsurada

Nandi

Zheng

et al. 2020

Cardiovasc Diabetol

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“…Attenuating NF-κB phosphorylation can inhibit inflammatory response after tissue ischemia. 40,41) Moreover, TGF-β/Smad signaling plays an important role in fibrosis, and Smad3's key role in TGF-β1-induced redundant accumulation of extracellular matrix (ECM) is comprehensively recognized. 42) Meanwhile, activation of mitogen-activated protein kinase (MAPK), including the ERK1/2, JNK1/2 and p38 pathways, can be involved in the pathological process of cardiac fibrosis as an upstream signaling molecule of Smad2/ 3.…”

Section: Discussionmentioning

confidence: 99%

Fisetin Alleviates Atrial Inflammation, Remodeling, and Vulnerability to Atrial Fibrillation after Myocardial Infarction

Liu

Shen

et al. 2019

Int. Heart J.

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Atrial inflammation and fibrosis are the critical processes involved in atrial fibrillation (AF) after myocardial infarction (MI). Fisetin is a dietary flavonoid that has shown forceful anti-inflammatory and antiproliferative properties in diverse models of disease. However, fisetin's role in atrial inflammation, fibrosis, and AF vulnerability post-MI remains completely unknown. Rats were subjected to MI surgery, by left anterior descending coronary artery ligation or sham operation, and treated with DMSO or fisetin via intraperitoneal injection. After 28 days, echocardiographic parameters were performed, and AF inducibility was tested. We further evaluated the inflammation, fibrosis of left atria (LA), and related signal pathways by RT-PCR, Western blot, and staining analysis. Compared to the MI group, fisetin treatment improved cardiac function, inhibited macrophage recruitment into the LA and production of IL-1β and TNF-α, and attenuated adverse atrial fibrosis following acute myocardial infarction (AMI). Electrophysiological recordings, using an isolated perfused heart, showed that MI-induced higher inducibility of AF and prolonged AF duration, interatrial conduction time (IACT), atrial effective refractory period (AERP) were significantly alleviated by fisetin. Mechanistically, fisetin markedly increased phosphorylated AMPK (p-AMPK) levels and suppressed NF-κB p65, p38MAPK, and smad3 phosphorylation in the LA post-MI. We demonstrate that fisetin improves LA expansion, cardiac function, atrial inflammation, fibrosis, and vulnerability to AF following MI by possibly regulating AMPK/NF-κB p65 and p38MAPK/smad3 signaling pathways.

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“…Sodium Houttuyfonate (SH), an addition compound from sodium bisulfite and houttuynin, has been used as a novel therapy for bronchitis and upper respiratory infections for years in China (See Supplementary Figure S1 for structure). Previously, it has been found that SH could block myocardial fibrosis to slow down or inhibit the progression of ventrical remodeling and heart failure induced by pressure overload in rats, by inhibiting the initiation of the renin-angiotensin-aldosterone system and decreasing production of collagen and the excretion of TNF-α (Gao et al, 2010;Zheng et al, 2018). Therefore, SH plays a role in fibrosis of viscera.…”

Section: Introductionmentioning

confidence: 99%

Sodium Houttuyfonate Inhibits Bleomycin Induced Pulmonary Fibrosis in Mice

et al. 2021

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Pulmonary fibrosis (PF) could severely disrupt the normal lung architecture and function with fatal consequences. Currently, there is no effective treatment for PF or idiopathic pulmonary fibrosis (IPF). The aim of this study was to investigate the effects of Sodium Houttuyfonate (SH) on bleomycin (BLM) induced PF mice model. Our results indicated that SH could attenuate BLM induced lung injury by reducing the inflammation, fibrogenesis and lung/body weight ratio. The proposed mechanisms for the protective effects of SH include: 1) improvement of pulmonary function in BLM mice, for instance, it can elevate the vital capacity (VC), increase the forced expiratory flow at 50% of forced vital capacity (FEF50) and improve other pulmonary function indices; 2) inhibition of collagen formation in BLM mice; 3) attenuation of the elevation of inflammatory cytokines, such as interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α), which are triggered by BLM administration; 4) reduction of the mRNA level and protein production of transforming growth factor-β1 (TGF-β1) in BLM mice. Furthermore, it was found that the protective effects of SH against BLM induced PF in mice was comparable to that of prednisone acetate (PA) tablets, a widely used drug for immunological diseases. Although Houttuynia Cordata Thunb has been widely used in China for lung infection and inflammation, the mechanism has not yet been fully elucidated. Our study provides the evidence that SH is an effective compound against pulmonary injury, irritation and fibrogenesis.

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Sodium Houttuyfonate Alleviates Post-infarct Remodeling in Rats via AMP-Activated Protein Kinase Pathway

Cited by 16 publications

References 25 publications

GLP-1 mediated diuresis and natriuresis are blunted in heart failure and restored by selective afferent renal denervation

GLP-1 mediated diuresis and natriuresis are blunted in heart failure and restored by selective afferent renal denervation

Fisetin Alleviates Atrial Inflammation, Remodeling, and Vulnerability to Atrial Fibrillation after Myocardial Infarction

Sodium Houttuyfonate Inhibits Bleomycin Induced Pulmonary Fibrosis in Mice

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