Gastrodin attenuation of the inflammatory response in H9c2 cardiomyocytes involves inhibition of NF-κB and MAPKs activation via the phosphatidylinositol 3-kinase signaling

Yang, Ping; Han, Yamei; Gui, Li; Sun, Jing; Chen, Yuan-li; Song, Rui; Guo, Jinming; Xie, Yanan; Lü, Di; Sun, Lin

doi:10.1016/j.bcp.2013.01.020

Cited by 104 publications

(65 citation statements)

References 36 publications

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“…NF‐κB is an essential transcriptional factor modulating inflammatory mediators and driving the expressions of iNOS and COX‐2 37. Evidence has emerged indicating that the iNOS and COX‐2 which regulated by NF‐κB are closely associated with the LPS‐induced myocardial disorder 38. Our experimental results suggested that Sal effectively inhibited the up‐regulations of iNOS, COX‐2 and p‐NF‐κB in LPS‐induced myocardial injury.…”

Section: Discussionmentioning

confidence: 58%

Salidroside suppressing LPS‐induced myocardial injury by inhibiting ROS‐mediated PI3K/Akt/mTOR pathway in vitro and in vivo

Chen

Liu

Feng

et al. 2017

J Cellular Molecular Medi

209

126

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The purpose of the present study was to investigate the effect of salidroside (Sal) on myocardial injury in lipopolysaccharide (LPS)‐induced endotoxemic in vitro and in vivo. SD rats were randomly divided into five groups: control group, LPS group (15 mg/kg), LPS plus dexamethasone (2 mg/kg), LPS plus Sal groups with different Sal doses (20, 40 mg/kg). Hemodynamic measurement and haematoxylin and eosin staining were performed. Serum levels of creatine kinase (CK), lactate dehydrogenase, the activities of the antioxidant enzymes catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH‐px), glutathione, tumour necrosis factor‐α (TNF‐α), interleukin‐6 (IL‐6), and interleukin‐1β (IL‐1β) were measured after the rats were killed. iNOS, COX‐2, NF‐κB and PI3K/Akt/mTOR pathway proteins were detected by Western blot. In vitro, we evaluated the protective effect of Sal on rat embryonic heart‐derived myogenic cell line H9c2 induced by LPS. Reactive oxygen species (ROS) in H9c2 cells was measured by flow cytometry, and the activities of the antioxidant enzymes CAT, SOD, GSH‐px, glutathione‐S‐transferase, TNF‐α, IL‐6 and IL‐1β in cellular supernatant were measured. PI3K/Akt/mTOR signalling was examined by Western blot. As a result, Sal significantly attenuated the above indices. In addition, Sal exerts pronounced cardioprotective effect in rats subjected to LPS possibly through inhibiting the iNOS, COX‐2, NF‐κB and PI3K/Akt/mTOR pathway in vivo. Furthermore, the pharmacological effect of Sal associated with the ROS‐mediated PI3K/Akt/mTOR pathway was proved by the use of ROS scavenger, N‐acetyl‐l‐cysteine, in LPS‐stimulated H9C2 cells. Our results indicated that Sal could be a potential therapeutic agent for the treatment of cardiovascular disease.

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Section: Discussionmentioning

confidence: 58%

Salidroside suppressing LPS‐induced myocardial injury by inhibiting ROS‐mediated PI3K/Akt/mTOR pathway in vitro and in vivo

Chen

Liu

Feng

et al. 2017

J Cellular Molecular Medi

209

126

View full text Add to dashboard Cite

show abstract

“…24 Stimulation of cells with LPS could induce the phosphorylation and activation of ERK1/2, JNK, and p38 MAPKs. 25,26 In this study, we detected the effects of TA on LPS-induced NF-kB and MAPK activation. The results showed that TA inhibited LPS-induced NF-kB and MAPK activation in a dose-dependent manner.…”

Section: Discussionmentioning

confidence: 98%

Tormentic acid inhibits LPS-induced inflammatory response in human gingival fibroblasts via inhibition of TLR4-mediated NF-κB and MAPK signalling pathway

Cao¹,

Zheng

et al. 2015

Archives of Oral Biology

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“…Fucosterol may be a useful agent for preventing LPS-induced ALI. Studies showed that inflammatory cytokines played critical roles in LPS-induced inflammatory response [16]. LPSinduced ALI is characterized by increased TNF-a, IL-1ß, and IL-6 levels in BALF [17].…”

Section: Discussionmentioning

confidence: 99%

Fucosterol attenuates lipopolysaccharide-induced acute lung injury in mice

Liu

et al. 2015

Journal of Surgical Research

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Gastrodin attenuation of the inflammatory response in H9c2 cardiomyocytes involves inhibition of NF-κB and MAPKs activation via the phosphatidylinositol 3-kinase signaling

Cited by 104 publications

References 36 publications

Salidroside suppressing LPS‐induced myocardial injury by inhibiting ROS‐mediated PI3K/Akt/mTOR pathway in vitro and in vivo

Salidroside suppressing LPS‐induced myocardial injury by inhibiting ROS‐mediated PI3K/Akt/mTOR pathway in vitro and in vivo

Tormentic acid inhibits LPS-induced inflammatory response in human gingival fibroblasts via inhibition of TLR4-mediated NF-κB and MAPK signalling pathway

Fucosterol attenuates lipopolysaccharide-induced acute lung injury in mice

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