Traditional Chinese medicine as a therapeutic option for cardiac fibrosis: Pharmacology and mechanisms

Li, Xiao; Li, Lin; Wei, Lei; Chua, Hui Zi; Li, Zining; Huang, Xianglong; Wang, Qilong; Li, Nan; Zhang, Han

doi:10.1016/j.biopha.2021.111979

Cited by 30 publications

(28 citation statements)

References 275 publications

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“…In addition, they are not suitable for long-term use ( 16 ). Although cardiac fibrosis is common, there are still no effective drugs to provide sufficient clinical intervention for cardiac fibrosis ( 37 ). New drugs and effective treatments are needed.…”

Section: Discussionmentioning

confidence: 99%

Clostridium butyricum and Bifidobacterium pseudolongum Attenuate the Development of Cardiac Fibrosis in Mice

Wang

Chen

et al. 2022

Microbiol Spectr

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Section: Discussionmentioning

confidence: 99%

Clostridium butyricum and Bifidobacterium pseudolongum Attenuate the Development of Cardiac Fibrosis in Mice

Wang

Chen

et al. 2022

Microbiol Spectr

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“…Nevertheless, the mechanisms of CF are unknown, and there is no efficacious treatment to halt the progression of CF [ 33 ]. A significant amount of research has focused on the therapeutic potential of TCM in the prevention and treatment of CF [ 34 ]. This study investigated whether QHF can achieve the antifibrosis effects in ISO-induced mice by regulating gut microbiota, intestinal integrity, and inflammation.…”

Section: Discussionmentioning

confidence: 99%

Qige Huxin Formula Attenuates Isoprenaline-Induced Cardiac Fibrosis in Mice via Modulating Gut Microbiota and Protecting Intestinal Integrity

Shi

Zuo

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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Background. The composition and metabolic activities of gut microbiota are strongly interconnected with cardiac fibrosis (CF) and heart failure (HF). Qige Huxin formula (QHF), a traditional Chinese medicine (TCM) formulation originating from a classical Fangji Huangqi decoction, has been widely used to clinically treat HF for decades. However, it is still unclear whether QHF alleviates CF by modulating gut microbiota and intestinal integrity. Purpose. This study aimed to investigate the cardioprotective effects of QHF in isoprenaline-induced CF through modulating gut microbiota and intestinal integrity. Methods. Fifty mice were randomly divided into five groups after one week of acclimatization feeding: control group, model group, 2.56 g/kg/d group (low-dose QHF), 5.12 g/kg/d group (high-dose QHF), and meto group (15 mg/kg/d). The CF model was established by subcutaneously injecting the mice with isoprenaline (10 mg/kg/d for 14 days), followed by QHF treatment. The heart volume, cardiac weight index (CWI), serum myocardial enzymes, serum inflammatory cytokines, serum lipopolysaccharide, histopathology of the heart and colon tissues, ZO-1, and occludin of colon tissues were then measured. Fecal samples from mice were analyzed using 16S rRNA sequencing. Results. QHF treatment significantly reduced heart volume, CWI, and serum CK and CK-MB levels, attenuated cardiac histopathological alterations, and alleviated CF. QHF treatment also downregulated TNF-α, IL-1β, and IL-6 in serum. Moreover, QHF treatment decreased the serum level of lipopolysaccharide and maintained intestinal integrity by upregulating ZO-1 and occludin. The 16S rRNA microbiota analysis revealed that QHF treatment increased the relative abundance of Marvinbryantia and Phascolarctobacterium. Conclusions. QHF treatment exerts cardioprotective effects through modulating gut microbiota, protecting intestinal integrity, and alleviating inflammation. This study shows that gut microbiota may enhance heart-gut interaction.

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“…In addition, myofibroblasts are differentiated from cardiac fibroblasts by myocardial injury, and the expression of alpha-SMA signals effective transformation into a phenotype with a high capacity to synthesize extracellular matrix proteins [76,77], and the fibrillary proteins which are the primary components of the cardiac extracellular matrix are type I collagen and type III collagen, which are considered as indicators of fibrosis in fibroblasts and then remodeling [76,78]. For that type I collagen, type III collagen and alpha-SMA expression promote thoracic and left ventricular remodeling [79][80][81][82]. The Salvia miltiorrhiza active ingredients have the effect of reducing the alpha-SMA expression, collagen, and ET-1, thereby reducing the vessel wall thickness [83].…”

Section: Discussionmentioning

confidence: 99%

GJD Modulates Cardiac/Vascular Inflammation and Decreases Blood Pressure in Hypertensive Rats

Mohammed

Liu

Baldi³

et al. 2022

Mediators of Inflammation

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Gedan Jiangya decoction (GJD) (aqueous ethanol extract), a traditional Chinese medicine formula which contain six botanical drugs (Uncaria rhynchophylla (Miq.) Miq., Salvia miltiorrhiza Bunge, Pueraria lobata (Willd.) Ohwi, Eucommia ulmoides Oliv., Prunella vulgaris L., and Achyranthes bidentata Blume) was designed to treat hypertension; however, the underlying mechanism of action is unclear. This study aimed to determine the mechanisms of action of GJD in the treatment of hypertension in spontaneously hypertensive rats (SHR). Male SHRs were randomly divided into five groups: GJD doses were low (1.36 g/kg/d), medium (2.72 g/kg/d), and high (5.44 g/kg/d), captopril (13.5 mg/kg/d), and SHR groups, with Wistar-Kyoto rats (WKY) serving as the control. Every rat was gavaged once a day. The ALC-NIBP, a noninvasive blood pressure device, measured systolic (SBP) and diastolic (DBP) blood pressures. Six weeks following treatment, all rats were anesthetized. The blood samples were obtained from the abdominal aorta and then serum isolated to assess endothelin-1 and angiotensin II, interleukin-1beta, interleukin-6, and TNF-alpha. The left ventricular and thoracic aortas were taken for HE staining, immunohistochemistry, RT-qPCR, and western blot examination. Following GJD therapy, SBP and DBP were significantly lowered, as were serum levels of endothelin-1 and angiotensin II. The thickness of the left ventricular and thoracic aorta walls reduced, as did type I collagen, type III collagen, and alpha-SMA expression in the left ventricular and aortic tissues. The GJD treatment significantly reduced serum levels of the inflammatory markers interleukin-1beta, interleukin-6, and TNF-alpha. Furthermore, interleukin-1 beta, interleukin-6, TNF-alpha, TAK1, and NF- κ B/p65 levels were significantly reduced in left ventricular and aortic tissues, whereas IkB-alpha levels were significantly elevated. GJD has a dose-dependent effect on all parameters. In conclusion, GJD has been shown to lower blood pressure, improve cardiovascular remodeling, and reduce inflammation via regulating NF- κ B in SHRs.

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Traditional Chinese medicine as a therapeutic option for cardiac fibrosis: Pharmacology and mechanisms

Cited by 30 publications

References 275 publications

Clostridium butyricum and Bifidobacterium pseudolongum Attenuate the Development of Cardiac Fibrosis in Mice

Clostridium butyricum and Bifidobacterium pseudolongum Attenuate the Development of Cardiac Fibrosis in Mice

Qige Huxin Formula Attenuates Isoprenaline-Induced Cardiac Fibrosis in Mice via Modulating Gut Microbiota and Protecting Intestinal Integrity

GJD Modulates Cardiac/Vascular Inflammation and Decreases Blood Pressure in Hypertensive Rats

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