Tanshinone IIA inhibits lipopolysaccharide‑induced inflammatory responses through the TLR4/TAK1/NF‑κB signaling pathway in vascular smooth muscle cells

Meng, Zhe; Si, Chun‐Ying; Teng, Shuai; Yu, Xin-hui; Li, Haiyu

doi:10.3892/ijmm.2019.4100

Cited by 11 publications

(14 citation statements)

References 44 publications

(50 reference statements)

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“…50 The TNF-α is an inflammatory cytokine and its expression level reflects the pathogenesis and severity of the inflammatory process. According to Meng et al, 51 in-vitro study, in VSMCs, LPS-induced inflammatory responses were found to be inhibited via tan-IIA by partially suppressed TLR4/TAK1/NF-κB signaling cascade. The results showed that by using tan-IIA, the neuronal TLR-4 and NF-κB expression levels were found to be reduced, while inflammatory cytokines production and neuronal oxidative stress levels were found to be elevated.…”

Section: Inflammation-related Signal Transduction Pathway Toll-like Receptor/nf-κb Pathwaymentioning

confidence: 98%

Pharmacological Activity and Mechanism of Tanshinone IIA in Related Diseases

Guo

et al. 2020

DDDT

190

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Salvia miltiorrhiza : (Danshen) is a significant (traditional Chinese medication) natural remedy, enhancing blood circulation and clear blood stasis. In this view, it is widely used against several heart diseases, eg, cardiomyopathy, arrhythmia, and congenital heart defects. Tanshinone IIA (tan-IIA) is the main fat-soluble component of Salvia miltiorrhiza . Modern pharmacological study shows that tan-IIA has anti-inflammatory and anti-oxidant activities. Tan-IIA induces remarkable cardioprotective effects via enhancing angiogenesis which may serve as an effective treatment against cardiovascular diseases (CVD). There is also evidence that tan-IIA has extensive immunomodulatory effects and plays a significant role in the development and function of immune cells. Tan-IIA reduces the production of inflammatory mediators and restores abnormal signaling pathways via regulating the function and activation of immune cells. It can also regulate signal transduction pathways, ie, TLR/NF-κB pathway and MAPKs/NF-κB pathway, thereby tan-IIA has an anti-inflammatory, anticoagulant, antithrombotic and neuroprotective role. It plays a protective role in the pathogenesis of cardiovascular disorders (ie, atherosclerosis, hypertension) and Alzheimer’s disease. It has also been revealed that tan-IIA has an anti-tumor role by killing various tumor cells, inducing differentiation and apoptosis, and has potential activity against carcinoma progression. In the review of this fact, the tan-IIA role in different diseases and its mechanism have been summarized while its clinical applications are also explored to provide a new perspective of Salvia miltiorrhiza . An extensive study on the mechanism of action of tan-IIA is of great significance for the effective use of Chinese herbal medicine and the promotion of its status and influence on the world.

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Section: Inflammation-related Signal Transduction Pathway Toll-like Receptor/nf-κb Pathwaymentioning

confidence: 98%

Pharmacological Activity and Mechanism of Tanshinone IIA in Related Diseases

Guo

et al. 2020

DDDT

190

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“…Tanshinone IIA (Tan IIA) is a lipophilic components deriving from the roots of Chinese herbs medicine Salvia miltiorrhiza Bunge 17. Tan IIA has been found to possess a number of biological activities, such as anti-inflammation, anti-oxidant and anti-tumor activities 18–20. Liu et al found that Tan IIA significantly inhibited the tumor growth of A549 human NSCLC xenografts 21.…”

Section: Introductionmentioning

confidence: 99%

“…17 Tan IIA has been found to possess a number of biological activities, such as anti-inflammation, anti-oxidant and anti-tumor activities. [18][19][20] Liu et al found that Tan IIA significantly inhibited the tumor growth of A549 human NSCLC xenografts. 21 Meanwhile, Tan IIA could induce apoptosis in NSCLC cells via downregulation the level of p-Akt.…”

Section: Introductionmentioning

confidence: 99%

Tanshinone IIA Reverses Gefitinib-Resistance In Human Non-Small-Cell Lung Cancer Via Regulation Of VEGFR/Akt Pathway

Wang¹,

Luo²,

Zhang³

et al. 2019

OTT

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BackgroundGefitinib-resistance is a primary obstacle for the treatment of non-small-cell lung cancer (NSCLC). It has been shown that tanshinone IIA (Tan IIA) could induce apoptosis of NSCLC cells. However, the role of combination of gefitinib with Tan IIA on gefitinib-resistance NSCLC cells remains unclear. Thus, this study aimed to investigate the role of combination on the proliferation, apoptosis and invasion of gefitinib-resistance NSCLC cells.MethodsCCK-8, flow cytometric and transwell assays were applied to detect proliferation, apoptosis and invasion in gefitinib-resistance NSCLC cells, respectively. In addition, Western blotting assay was used to detect the expressions of p-EGFR, p-VEGFR2, and p-Akt in HCC827/gefitinib cells.ResultsIn this study, Tan IIA enhanced the cytotoxic effect of gefitinib in gefitinib-resistance NSCLC cells. In addition, the inhibitory effects of gefitinib on the proliferation, migration and invasion of gefitinib-resistance NSCLC cells were enhanced in the presence of Tan IIA. Moreover, Tan IIA enhanced the pro-apoptotic effect of gefitinib in gefitinib-resistance NSCLC cells via increasing the level of cleaved caspase 3. Meanwhile, Tan IIA enhanced the sensitivity of HCC827/gefitinib cells to gefitinib via downregulation of the VEGFR2/Akt pathway. In vivo experiments further confirmed that combination of gefitinib with Tan IIA inhibited tumor growth in mouse xenograft model of HCC827/gefitinib.ConclusionWe found that Tan IIA could enhance gefitinib sensitivity in gefitinib-resistance NSCLC cells. Therefore, combination of gefitinib with Tan IIA might be considered as a therapeutic approach for the treatment of gefitinib-resistant NSCLC.

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“…To date, TLR2 and TLR4 have been increasingly recognized to share common pathways, eliciting synergetic effects on inflammatory responses such as vascular inflammation [5]. Previous literature reported that IL-6 was modulated by TLR2-dependent NF-κB activation in VSMCs [16], and so was TLR4 [17]. Collectively, IL-6-driven vascular inflammation is tightly regulated by a complicated network of signaling pathways.…”

Section: Introductionmentioning

confidence: 99%

Carbon Monoxide‐Releasing Molecule‐2 Ameliorates Particulate Matter‐Induced Aorta Inflammation via Toll‐Like Receptor/NADPH Oxidase/ROS/NF‐κB/IL‐6 Inhibition

Hsu

Wee

et al. 2021

Oxidative Medicine and Cellular Longevity

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Particulate matter (PM), a major air pollutant, may be associated with adverse cardiovascular effects. Reactive oxygen species- (ROS-) dependent proinflammatory cytokine production, such as interleukin-6 (IL-6), is a possible underlying mechanism. Carbon monoxide- (CO-) releasing molecule-2 (CORM-2) which liberates exogenous CO can exert many beneficial effects, particularly anti-inflammation and antioxidant effects. The purpose of this study was to explore the protective effects and underpinning mechanisms of CORM-2 on PM-induced aorta inflammation. Here, human aortic vascular smooth muscle cells (HASMCs) were utilized as in vitro models for the assessment of signaling pathways behind CORM-2 activities against PM-induced inflammatory responses, including Toll-like receptors (TLRs), NADPH oxidase, ROS, nuclear factor-kappa B (NF-κB), and IL-6. The modulation of monocyte adherence and HASMC migration, that are two critical cellular events of inflammatory process, along with their regulators, including intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and matrix metalloproteinase-2 (MMP-2) and MMP-9, in response to PM by CORM-2, were further evaluated. Finally, mice experiments under different conditions were conducted for the in vivo evaluation of CORM-2 benefits on the expression of inflammatory molecules including IL-6, ICAM-1, VCAM-1, MMP-2, and MMP-9. Our results found that PM could induce aorta inflammation in vitro and in vivo, as evidenced by the increase of IL-6 expression that was regulated by the TLR2 and TLR4/NADPH oxidase/ROS/NF-κB signaling pathway, thereby promoting ICAM-1- and VCAM-1-dependent monocyte adhesion and MMP-2- and MMP-9-dependent HASMC migration. Importantly, our experimental models demonstrated that CORM-2-liberated CO effectively inhibited the whole identified PM-induced inflammatory cascade in HASMCs and tissues. In conclusion, CORM-2 treatment may elicit multiple beneficial effects on inflammatory responses of aorta due to PM exposure, thereby providing therapeutic value in the context of inflammatory diseases of the cardiovascular system.

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Tanshinone IIA inhibits lipopolysaccharide‑induced inflammatory responses through the TLR4/TAK1/NF‑κB signaling pathway in vascular smooth muscle cells

Cited by 11 publications

References 44 publications

<p>Pharmacological Activity and Mechanism of Tanshinone IIA in Related Diseases</p>

<p>Pharmacological Activity and Mechanism of Tanshinone IIA in Related Diseases</p>

<p>Tanshinone IIA Reverses Gefitinib-Resistance In Human Non-Small-Cell Lung Cancer Via Regulation Of VEGFR/Akt Pathway</p>

Carbon Monoxide‐Releasing Molecule‐2 Ameliorates Particulate Matter‐Induced Aorta Inflammation via Toll‐Like Receptor/NADPH Oxidase/ROS/NF‐κB/IL‐6 Inhibition

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