Salidroside Mitigates Sepsis-Induced Myocarditis in Rats by Regulating IGF-1/PI3K/Akt/GSK-3β Signaling

He, He; Chang, Xiayun; Gao, Jin; Zhu, Lingpeng; Miao, Ming; Yan, Tianhua

doi:10.1007/s10753-015-0200-7

Cited by 53 publications

(34 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous research proved that the elevated levels of inflammatory markers were associated with myocardial ischemia [24]. The inflammatory stresses induced by ISO were indicated by serum IL-6, IL-1β and TNF-α elevations [25].…”

Section: Discussionmentioning

confidence: 96%

Crocetin ester improves myocardial ischemia via Rho/ROCK/NF-κB pathway

Huang

Chen

Wang

et al. 2016

International Immunopharmacology

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 96%

Crocetin ester improves myocardial ischemia via Rho/ROCK/NF-κB pathway

Huang

Chen

Wang

et al. 2016

International Immunopharmacology

View full text Add to dashboard Cite

“…I/R increases the local or systemic release of proinflammatory cytokines, including TNF-α, IL-1β and IL-6, and further increases cardiac injury, and inhibition of the I/R-induced inflammatory response alleviates myocardial I/R injury (45,46). It has been previously hypothesized that salidroside may exhibit a protective effect on myocardial injury by inhibiting the inflammatory response (11,14,47). In vitro and in vivo experiments have demonstrated that miR-21 regulated the production of various important pro-inflammatory cytokines secreted during I/R injury (48,49).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑21 mediates the protective effects of salidroside against hypoxia/reoxygenation‑induced myocardial oxidative stress and inflammatory response

Liu

Wei²,

Lan

et al. 2020

Exp Ther Med

View full text Add to dashboard Cite

Myocardial ischemia-reperfusion (I/R) injury is the oxidative stress and inflammatory response that occurs when a tissue is reperfused following a prolonged period of ischemic injury. Growing evidence has demonstrated that microRNAs (miRs) are essential in the development of myocardial I/R injury. Salidroside, a phenylpropanoid glycoside isolated from a traditional Chinese medicinal plant, Rhodiola rosea, possesses multiple pharmacological functions and protects against myocardial I/R injury in vitro and in vivo. However, the role of miRs in the cardioprotective effects of salidroside against myocardial I/R injury has not been studied, to the best of our knowledge. In the present study, the role of miR21 in the underlying mechanism of salidroside-induced protection against oxidative stress and inflammatory injuries in hypoxia/reoxygenation (H/R)-treated H9c2 cardiomyocytes was determined. The cell viability was assessed with an MTT assay. Lactate dehydrogenase (LDH) release, caspase-3 activity, malondialdehyde (MDA) level, superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities were determined by commercial kits. Cell apoptosis was measured by flow cytometry. Intracellular reactive oxygen species (ROS) generation was monitored by DCFH-DA. The miR-21 level was quantified by reverse transcription-quantitative (RT-q)PCR. The interleukin (IL)-6, IL-1β and tumor necrosis factor (TNF)-α levels were measured by RT-qPCR and ELISA. The results showed that salidroside pretreatment significantly increased cell viability and decreased the release of LDH, accompanied by an increase in miR-21 expression in H/R-treated H9c2 cells and a miR-21 inhibitor reversed these effects. In addition, the miR-21 inhibitor also abrogated the inhibition of salidroside on H/R-induced increases in apoptosis and caspase-3 activity in H9c2 cells. Salidroside mitigated H/R-induced oxidative stress as illustrated by the downregulation of ROS generation and MDA level and increased the activities of the antioxidant enzymes, SOD and GSH-Px, all of which were abrogated in cells transfected with the miR-21 inhibitor. Salidroside induced a decrease in the expression and levels of the pro-inflammatory cytokines, IL-6, IL-1β and TNF-α, which were prevented by the miR-21 inhibitor. Together, these results provide evidence of the beneficial effects of salidroside against myocardial I/R injury by reducing myocardial oxidative stress and inflammation which are enhanced by increasing miR-21 expression.

show abstract

“…Patients with heart injury have increased levels of cardiac marker enzymes in serum, which are often measured as indicators of heart disease in the clinic. CK and LDH are cardiac marker enzymes, which play a pivotal role in energy metabolism and membrane permeability in the heart (He et al, 2015). Previous studies have indicated that LPS can induce heart injury, which is characterized by the elevation of CK and LDH in serum.…”

Section: Discussionmentioning

confidence: 99%

Protective effects of rutin on lipopolysaccharide-induced heart injury in mice

Xianchu¹,

Zheng²,

Liu³

et al. 2018

J. Toxicol. Sci.

View full text Add to dashboard Cite

Rutin has a wide range of beneficial health properties in the amelioration of multi-organ injury owing to its various biological effects. The aim of this study was to investigate the effects of rutin on lipopolysaccharide (LPS)-induced heart injury and clarify its potential cardioprotective mechanism. The mouse model of heart injury was intraperitoneal infection with LPS, and rutin was orally administered for 8 consecutive days. One day after LPS injection, heart histopathology, cardiac marker enzymes and cardiac fibrosis related genes were determined to evaluate the cardioprotective effects of rutin. In addition, oxidative parameters and inflammatory cytokines were tested to explore its possible underlying mechanism. The presented results showed that rutin significantly improved morphological changes of myocardium and relieved cardiac marker enzymes [creatine kinase (CK) and lactate dehydrogenase (LDH)] level to protect heart in LPS-induced sepsis. And more, rutin observably mitigated fibrosis related genes [matrix metalloproteinase 2 (MMP-2) and matrix metalloproteinase 9 (MMP-9)] expression in the heart to prevent against LPS-induced cardiac fibrosis. In addition, rutin markedly increased antioxidant enzymes [superoxide dismutase (SOD) and catalase (CAT)] activity, and improved oxidative production [malondialdehyde (MDA) and HO] level to balance the oxidation and anti-oxidation systems in the heart. Lastly, rutin dramatically ameliorated [tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6)] activity to restrain inflammatory responses in the heart. In conclusion, rutin possessed anti-oxidant and anti-inflammatory properties to improve LPS-induced heart injury, which suggested rutin could be used as a potential cardioprotective medicine in sepsis.

show abstract

Salidroside Mitigates Sepsis-Induced Myocarditis in Rats by Regulating IGF-1/PI3K/Akt/GSK-3β Signaling

Cited by 53 publications

References 25 publications

Crocetin ester improves myocardial ischemia via Rho/ROCK/NF-κB pathway

Crocetin ester improves myocardial ischemia via Rho/ROCK/NF-κB pathway

MicroRNA‑21 mediates the protective effects of salidroside against hypoxia/reoxygenation‑induced myocardial oxidative stress and inflammatory response

Protective effects of rutin on lipopolysaccharide-induced heart injury in mice

Contact Info

Product

Resources

About