Buyanghuanwu Decoction alleviated pressure overload induced cardiac remodeling by suppressing Tgf-β/Smads and MAPKs signaling activated fibrosis

Chen, Huihua; Song, Haiyan; Liu, Xiao; Tian, Jing; Tang, Wenzhu; Cao, T.; Zhao, Pei; Zhang, Chen; Guo, Wei; Xu, Ming; Lü, Rong

doi:10.1016/j.biopha.2017.08.102

Cited by 27 publications

(11 citation statements)

References 21 publications

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“…Liuweiwuling tablets were supported by the inhibition of the TGF-β/Smad-mediated synthesis of collagen I in hepatic fibrosis [121]. Buyanghuanwu decoction is a representative prescription for the treatment of qi-deficiency and blood-stasissyndrome and Buyanghuanwu decoction exerted a cardioprotective effect against pressure overload induced cardiac remodeling via inactivation of TGF-β/Smad signaling triggered fibrosis [122].…”

Section: Targeting Tgf-β1/smad Signaling By Extracts and Compound Prementioning

confidence: 99%

New insights into TGF-β/Smad signaling in tissue fibrosis

Chen

Wang

et al. 2018

Chemico-Biological Interactions

787

480

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Transforming growth factor-β1 (TGF-β1) is considered as a crucial mediator in tissue fibrosis and causes tissue scarring largely by activating its downstream small mother against decapentaplegic (Smad) signaling. Different TGF-β signalings play different roles in fibrogenesis. TGF-β1 directly activates Smad signaling which triggers pro-fibrotic gene overexpression. Excessive studies have demonstrated that dysregulation of TGF-β1/Smad pathway was an important pathogenic mechanism in tissue fibrosis. Smad2 and Smad3 are the two major downstream regulator that promote TGF-β1-mediated tissue fibrosis, while Smad7 serves as a negative feedback regulator of TGF-β1/Smad pathway thereby protects against TGF-β1-mediated fibrosis. This review presents an overview of the molecular mechanisms of TGF-β/Smad signaling pathway in renal, hepatic, pulmonary and cardiac fibrosis, followed by an in-depth discussion of their molecular mechanisms of intervention effects both in vitro and in vivo. The role of TGF-β/Smad signaling pathway in tumor or cancer is also discussed. Additionally, the current advances also highlight targeting TGF-β/Smad signaling pathway for the prevention of tissue fibrosis. The review reveals comprehensive pathophysiological mechanisms of tissue fibrosis. Particular challenges are presented and placed within the context of future applications against tissue fibrosis.

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Section: Targeting Tgf-β1/smad Signaling By Extracts and Compound Prementioning

confidence: 99%

New insights into TGF-β/Smad signaling in tissue fibrosis

Chen

Wang

et al. 2018

Chemico-Biological Interactions

787

480

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“…Carthamus tinctorius L. (Honghua), a dried flower, often used to promote blood circulation, dispel blood stasis, and relieve pain [8,9]. Huangqi-Honghua (HH) herb pair has been used widely in clinical practice for treating Qi deficiency and blood stasis syndrome, especially cerebrovascular and cardiovascular diseases, with a long history, such as Buyang Huanwu decoction, a wellknown TCM formula [10][11][12]. In our previous study, by using a rat model of middle cerebral artery occlusion (MCAO), we have validated the synergetic effect of hydroxysafflor yellow A and astragaloside IV (main constituents of HH) in removing blood stasis (QDBS) syndrome [13].…”

Section: Introductionmentioning

confidence: 99%

A Network Pharmacology Approach to Predict the Proangiogenesis Mechanism of Huangqi-Honghua Herb Pair after Cerebral Ischemia

Cao

Lü

Wang

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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Objective. Huangqi-Honghua herb pair is known for its medicinal value to treat Qi deficiency and blood stasis syndrome with a long history in clinical practice. To understand its possible mechanism in a systematic study, a network pharmacological method was addressed. Methods. Detailed information on the HH compounds was obtained from two public databases, and oral bioavailability (OB) and drug-like (DL) of the compounds were evaluated. A correlation between HH compounds, its potential targets, and known targets was extrapolated, and the herb-compound-target-disease (H-C-T-D) network was established. Next, the pathway enrichment and essential genes were analyzed. Then, three key genes (VEGFA, VEGFR2, and eNOS), highly associated with angiogenesis, were screened and verified through western blot assay. Results. Out of 276 compounds, 21 HH compounds and 78 target genes regulating the major pathways associated with CI in the network are analyzed. The bioactive compounds in HH were active in various signal transduction pathways such as the toll-like receptor signaling pathway, VEGF signaling pathway, TNF signaling pathway, and HIF-1 signaling pathway are important pathways that may regulate anti-inflammatory, antiapoptotic, immune correlation, and antioxidative effects. The core genes are PTGS2, TNF, NOS2, IL6, BCL2, IL1B, SOD2, NOS3, SOD1, MMP9, and VEGFA. The in vitro results suggested that HH treatment could significantly elevate the expression of proangiogenic genes such as VEGFA, VEGFR2, and eNOS compared with OGD groups. Conclusions. Our results predict that HH may regulate the expression of VEGFA, VEGFR2, and eNOS via the VEGF and HIF-1 signaling pathway to promote angiogenesis and alleviate cerebral ischemia injury.

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“…e MAPK signaling pathway could be a promising candidate for future applications in CNS injury treatment [68]. BHD alleviated pressure overload induced cardiac remodeling by suppressing TGF-β/Smads and MAPKs signaling activated fibrosis [69].…”

Section: Discussionmentioning

confidence: 99%

Network Pharmacology and Molecular Docking Analysis on Molecular Targets and Mechanisms of Buyang Huanwu Decoction in the Treatment of Ischemic Stroke

Gao

Tian

Han

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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Background and Objective. With the exact clinical efficacy, Buyang Huanwu decoction (BHD) is a classical prescription for the treatment of ischemic stroke (IS). Here, we aimed to investigate the pharmacological mechanisms of BHD in treating IS using systems biology approaches. Methods. The bioactive components and potential targets of BHD were screened by TCMSP, BATMAN-TCM, ETCM, and SymMap databases. Besides, compounds that failed to find the targets from the above databases were predicted through STITCH, SwissTargetPrediction, and SEA. Moreover, six databases were searched to mine targets of IS. The intersection targets were obtained and analyzed by GO and KEGG enrichment. Furthermore, BHD-IS PPI network, compound-target network, and herb-target-pathway network were constructed by Cytoscape 3.6.0. Finally, AutoDock was used for molecular docking verification. Results. A total of 235 putative targets were obtained from 59 active compounds in BHD. Among them, 62 targets were related to IS. PPI network showed that the top ten key targets were IL6, TNF, VEGFA, AKT1, etc. The enrichment analysis demonstrated candidate BHD targets were more frequently involved in TNF, PI3K-Akt, and NF-kappa B signaling pathway. Network topology analysis showed that Radix Astragali was the main herb in BHD, and the key components were quercetin, beta-sitosterol, kaempferol, stigmasterol, etc. The results of molecular docking showed the active components in BHD had a good binding ability with the key targets. Conclusions. Our study demonstrated that BHD exerted the effect of treating IS by regulating multitargets and multichannels with multicomponents through the method of network pharmacology and molecular docking.

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Buyanghuanwu Decoction alleviated pressure overload induced cardiac remodeling by suppressing Tgf-β/Smads and MAPKs signaling activated fibrosis

Cited by 27 publications

References 21 publications

New insights into TGF-β/Smad signaling in tissue fibrosis

New insights into TGF-β/Smad signaling in tissue fibrosis

A Network Pharmacology Approach to Predict the Proangiogenesis Mechanism of Huangqi-Honghua Herb Pair after Cerebral Ischemia

Network Pharmacology and Molecular Docking Analysis on Molecular Targets and Mechanisms of Buyang Huanwu Decoction in the Treatment of Ischemic Stroke

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