Salidroside rescued mice from experimental sepsis through anti-inflammatory and anti-apoptosis effects

Liu, Shanshan; Yu, Xiaoyan; Hu, Baoji; Zou, Yun; Li, Jinbao; Bo, Lulong; Deng, Xiaoming

doi:10.1016/j.jss.2015.01.021

Cited by 31 publications

(16 citation statements)

References 28 publications

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“…In a LPS-induced acute lung injury(ALI) model, salidroside exerted anti-inflammatory effect via down-regulating the activation of JAK2-STAT3 pathway and suppressing STAT3 transfer into the nucleus in part [20]. In septic mice, Liu et al show that salidroside administration prolongs the survival, alleviates the pathologic lung changes and preserves adaptive immunity [21]. Likewise, in an ovalbumin (OVA)-induced asthma model, after treatment of salidroside, the airway hyper-reactivity virtually eliminates, the eosinophil percent markedly reduces, the level of IL-4 reduces and INF-γ obviously raises, and this is related to the regulation of Th1/Th2 balance [22].…”

Section: Discussionmentioning

confidence: 99%

Salidroside Attenuates Ventilation Induced Lung Injury via SIRT1-Dependent Inhibition of NLRP3 Inflammasome

Wang

Liu

et al. 2017

Cell Physiol Biochem

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Background: Salidroside (SDS) is the main effective ingredient of Rhodiola rosea L with a variety of pharmacologic properties. We aim to investigate the effects of SDS on ventilation induced lung injury (VILI) and explore the possible underlying molecular mechanism. Methods: Lung injury was induced in male ICR mice via mechanical ventilation (30 ml/kg) for 4h. The mice were divided in four groups:(1) Control group; (2) Ventilation group; (3) SDS group; (4) Ventilation with SDS group. SDS (50 mg/kg) was injected intraperitoneally 1h before operation. Mouse lung vascular endothelial cells (MLVECs) were subjected to cyclic stretch for 4h. Results: It was found that SDS attenuated VILI as shown in HE staining, cell count and protein content levels in BAL fluid, W/D and Evans blue dye leakage into the lung tissue. SDS treatment inhibited the activation of NLRP3 inflammasome and subsequent caspase-1 cleavage as well as interleukin (IL)-1β secretion both in vivo and in vitro. Moreover, SDS administration up-regulated SIRT1 expression. Importantly, knockdown of SIRT1 reversed the inhibitory effect of SDS on NLRP3 inflammasome activation. Conclusions: Taken together, these findings indicate that SDS may confer protection against ventilation induced lung injury via SIRT1-de-pendent inhibition of NLRP3 inflammasome activation.

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Section: Discussionmentioning

confidence: 99%

Salidroside Attenuates Ventilation Induced Lung Injury via SIRT1-Dependent Inhibition of NLRP3 Inflammasome

Wang

Liu

et al. 2017

Cell Physiol Biochem

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“…Salidroside has the effects of anti-hypoxia, anti-inflammatory, anti-apoptosis, anti-cancer and so on [24,25]. In this study, we detected the effects of salidroside on oxidative stress in the brain tissue of rats.…”

Section: Discussionmentioning

confidence: 84%

Salidroside regulates imbalance of Th17/Treg and promotes ischemic tolerance by targeting STAT-3 in cerebral ischemia-reperfusion injury

et al. 2021

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IntroductionThe balance between Th17 and Treg cells controls the immune response and is an important regulator of helper T cells acting on autoimmune diseases. Focal cerebral ischemia-reperfusion injury can induce imbalance of Th17/Treg cells in the brain and the peripheral immune system of rats. The aim of this study was to investigate the effect of salidroside (Sal) on the ratio of Th17 and Treg cells in an adult rat model of middle cerebral artery occlusion (MCAO).Material and methodsForty rats were divided into 4 groups: normal group, sham group, surgery group, and Sal group. After treatment, the neurological deficits in rats were evaluated. Peripheral blood mononuclear cells were isolated and the count of Th17 and Treg cells was detected by flow cytometry. The infarct size and expression of RORt and Foxp3 were detected in rat brain tissue. Rat spleen cells were isolated, CD4+ T cells were purified by immunomagnetic beads. Treg cells were induced by adding cytokine TGF-. Th17 cells were induced by adding cytokine IL-6. The expression of STAT-3 was inhibited by SiRNA, and the effect of Sal on the differentiation of Th17/Treg cells was analyzed. The expression levels of IL-6, TNF-, MCP-1, STAT-3 and NF--B2 proteins were examined.ResultsThe results show that MCAO can induce an imbalance of Th17 and Treg cells in peripheral blood of rats. Sal treatment can significantly reduce the neurological deficit and infarct size of MCAO rats, reverse the oxidative stress of rat brain tissue, and inhibit the apoptosis of brain cells in MCAO rats. In the brain tissue of MCAO rats, Sal could significantly inhibit the expression of IL-6, TNF-, MCP-1, STAT-3 and NF--B2. Down-regulation of STAT-3 significantly reversed the therapeutic effects of Sal treatment.ConclusionsOur results indicate that Sal can increase the tolerance of rat brain tissue to ischemia, inhibit cell apoptosis and reduce oxidative stress by targeting STAT-3.

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“…Salidroside also improved the survival and inhibited the proinflammatory responses during sepsis. 11 However, the effects of salidroside on IL-1β-stimulated OA chondrocytes remain to be elucidated. This study aimed to evaluate the antiinflammatory effects of salidroside on IL-1β-stimulated human OA chondrocytes and explore its underlying mechanisms.…”

Section: Introductionmentioning

confidence: 99%

Salidroside attenuates interleukin‐1β‐induced inflammation in human osteoarthritis chondrocytes

Zhang

Zhao

2018

J of Cellular Biochemistry

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Salidroside, a bioactive constituent isolated from Rhodiola rosea, has been reported to have anti‐inflammatory effects. However, the effects of salidroside on interleukin (IL)‐1β‐stimulated osteoarthritis (OA) chondrocytes remain to be elucidated. Thus, this study aimed to evaluate the anti‐inflammatory effects of salidroside on IL‐1β‐stimulated human OA chondrocytes and explore its underlying mechanisms. Our results showed that salidroside significantly inhibited the production of nitric oxide and prostaglandin E‐2, as well as suppressed the expression of inducible nitric oxide synthase and cyclooxygenase‐2 in IL‐1β‐stimulated chondrocytes ( P < .05). In addition, salidroside also suppressed IL‐1β‐induced matrix metalloproteinases production in human OA chondrocytes ( P < .05). Furthermore, pretreatment with salidroside prevented IL‐1β‐induced NF‐κB activation in OA chondrocytes ( P < .05). In conclusion, the current study demonstrated that salidroside inhibited the IL‐1β‐induced inflammatory response in OA chondrocytes via inhibition of NF‐κB activation.

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Salidroside rescued mice from experimental sepsis through anti-inflammatory and anti-apoptosis effects

Cited by 31 publications

References 28 publications

Salidroside Attenuates Ventilation Induced Lung Injury via SIRT1-Dependent Inhibition of NLRP3 Inflammasome

Salidroside Attenuates Ventilation Induced Lung Injury via SIRT1-Dependent Inhibition of NLRP3 Inflammasome

Salidroside regulates imbalance of Th17/Treg and promotes ischemic tolerance by targeting STAT-3 in cerebral ischemia-reperfusion injury

Salidroside attenuates interleukin‐1β‐induced inflammation in human osteoarthritis chondrocytes

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