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TSPO ligands prevent the proliferation of vascular smooth muscle cells and attenuate neointima formation through AMPK activation.
In this study we investigated the role of endogenous TSPO in neointima formation after angioplasty in vitro and in vivo. We established a vascular injury model in vitro by using platelet-derived growth factor-BB (PDGF-BB) to stimulate rat thoracic aortic smooth muscle cells (A10 cells). We found that treatment with PDGF-BB (1-20 ng/mL) dose-dependently increased TSPO expression in A10 cells, which was blocked in the presence of PKC inhibitor or MAPK inhibitor. Overexpression of TSPO significantly promoted the proliferation and migration in A10 cells, whereas downregulation of TSPO expression by siRNA or treatment with TS...
Source: Acta Pharmacologica Sinica - September 11, 2019 Category: Drugs & Pharmacology Authors: Wu LP, Gong ZF, Wang H, Zhou ZS, Zhang MM, Liu C, Ren HM, Yang J, Han Y, Zeng CY Tags: Acta Pharmacol Sin Source Type: research

Ability to Suppress TGF- β-Activated Myofibroblast Differentiation Distinguishes the Anti-pulmonary Fibrosis Efficacy of Two Danshen-Containing Chinese Herbal Medicine Prescriptions
Conclusion: This study suggests that a clinically efficacious cardiovascular Chinese herbal medicine (DLP) can be successfully repurposed to treat a lung disease in pulmonary fibrosis guided by TCM theory. Our comparative study between DLP and DHP demonstrated a critical requirement of suppressing both pro-inflammatory and pro-fibrotic pathways for the treatment of pulmonary fibrosis, supporting that a multi-component prescription capable of “removing both phlegm and blood stasis” will better achieve co-protection of heart and lung in PHD. Introduction Idiopathic pulmonary fibrosis (IPF) is a chronic ...
Source: Frontiers in Pharmacology - April 23, 2019 Category: Drugs & Pharmacology Source Type: research

Role of high mobility group A1/nuclear factor-kappa B signaling in coronary microembolization-induced myocardial injury.
CONCLUSIONS: HMGA1/NF-κB signaling is involved in CME-induced myocardial inflammation. Inhibition of HMGA1/NF-κB signaling attenuated the CME-induced myocardial injury and improved cardiac function, suggesting a new potential target for the prevention and treatment of CME-induced myocardial injury. PMID: 30021353 [PubMed - in process]
Source: Biomedicine and pharmacotherapy = Biomedecine and pharmacotherapie - July 21, 2018 Category: Drugs & Pharmacology Authors: Su Q, Lv X, Sun Y, Yang H, Ye Z, Li L Tags: Biomed Pharmacother Source Type: research

Role of high mobility group A1/nuclear factor-kappa B signaling in coronary microembolization-induced myocardial injury
ConclusionsHMGA1/NF-κB signaling is involved in CME-induced myocardial inflammation. Inhibition of HMGA1/NF-κB signaling attenuated the CME-induced myocardial injury and improved cardiac function, suggesting a new potential target for the prevention and treatment of CME-induced myocardial injury.Graphical abstract
Source: Biomedicine and Pharmacotherapy - July 10, 2018 Category: Drugs & Pharmacology Source Type: research

AdipoRon, an adiponectin receptor agonist, attenuates PDGF-induced VSMC proliferation through inhibition of mTOR signaling independent of AMPK: Implications toward suppression of neointimal hyperplasia
Publication date: May 2017 Source:Pharmacological Research, Volume 119 Author(s): Arwa Fairaq, Noha M. Shawky, Islam Osman, Prahalathan Pichavaram, Lakshman Segar Hypoadiponectinemia is associated with an increased risk of coronary artery disease. Although adiponectin replenishment mitigates neointimal hyperplasia and atherosclerosis in mouse models, adiponectin therapy has been hampered in a clinical setting due to its large molecular size. Recent studies demonstrate that AdipoRon (a small-molecule adiponectin receptor agonist) improves glycemic control in type 2 diabetic mice and attenuates postischemic cardiac injury i...
Source: Pharmacological Research - March 6, 2017 Category: Drugs & Pharmacology Source Type: research

Sulforaphane inhibits platelet-derived growth factor-induced vascular smooth muscle cell proliferation by targeting mTOR/p70S6kinase signaling independent of Nrf2 activation
Publication date: May 2017 Source:Pharmacological Research, Volume 119 Author(s): Noha M. Shawky, Lakshman Segar Activation of nuclear factor erythroid 2-related factor 2 (Nrf2, a transcription factor) and/or inhibition of mammalian target of rapamycin (mTOR) are implicated in the suppression of vascular smooth muscle cell (VSMC) proliferation. The present study has examined the likely regulatory effects of sulforaphane (SFN, an antioxidant) on Nrf2 activation and platelet-derived growth factor (PDGF)-induced mTOR signaling in VSMCs. Using human aortic VSMCs, nuclear extraction and siRNA-mediated downregulation studies we...
Source: Pharmacological Research - February 23, 2017 Category: Drugs & Pharmacology Source Type: research

Pioglitazone, a PPARγ agonist, attenuates PDGF-induced vascular smooth muscle cell proliferation through AMPK-dependent and AMPK-independent inhibition of mTOR/p70S6K and ERK signaling.
Abstract Pioglitazone (PIO), a PPARγ agonist that improves glycemic control in type 2 diabetes through its insulin-sensitizing action, has been shown to exhibit beneficial effects in the vessel wall. For instance, it inhibits vascular smooth muscle cell (VSMC) proliferation, a major event in atherosclerosis and restenosis after angioplasty. Although PPARγ-dependent and PPARγ-independent mechanisms have been attributed to its vasoprotective effects, the signaling events associated with PIO action in VSMCs are not fully understood. To date, the likely intermediary role of AMP-activated protein kinase (AMPK) towar...
Source: Biochemical Pharmacology - November 28, 2015 Category: Drugs & Pharmacology Authors: Osman I, Segar L Tags: Biochem Pharmacol Source Type: research