Neuroprotective effects of salidroside on focal cerebral ischemia/reperfusion injury involves the nuclear erythroid 2-related factor 2 pathway

Han, Jing; Xiao, Qing; Lin, Yansong; Zheng, Zhiyong; He, Zhaodong; Hu, Juan; Chen, Lidian

doi:10.4103/1673-5374.172317

Cited by 41 publications

(34 citation statements)

References 28 publications

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“…Salidroside, a natural compound extracted Rhodiola rosea L, which has long been used as a traditional Tibetan medicine to relieve altitude sickness, other effects on neuro-protection, cardio-protection, anti-depression, anti-fatigue, and anti-tumor have been reported [ 14 , 15 ]. Salidroside is thought to be one of the most effective compounds from Rhodiola rosea L for its multiple functions, such as anti-aging, anti-cancer, anti-inflammation, anti-oxidative stress, hepatoprotective properties and neuroprotective effect [ 31 – 36 ]. But the specific molecular target of salidroside has not been reported.…”

Section: Discussionmentioning

confidence: 99%

Salidroside suppresses solar ultraviolet-induced skin inflammation by targeting cyclooxygenase-2

Yuan

et al. 2016

Oncotarget

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Solar ultraviolet (SUV) irradiation causes skin disorders such as inflammation, photoaging, and carcinogenesis. Cyclooxygenase-2 (COX-2) plays a key role in SUV-induced skin inflammation, and targeting COX-2 may be a strategy to prevent skin disorders. In this study, we found that the expression of COX-2, phosphorylation of p38 or JNKs were increased in human solar dermatitis tissues and SUV-irradiated human skin keratinocyte HaCaT cells and mouse epidermal JB6 Cl41 cells. Knocking down COX-2 inhibited the production of prostaglandin E2 (PGE2), the phosphorylation of p38 or JNKs in SUV-irradiated cells, which indicated that COX-2 is not only the key enzyme for PGs synthesis, but also an upstream regulator of p38 or JNKs after SUV irradiation. The virtual ligand screening assay was used to search for natural drugs in the Chinese Medicine Database, and indicated that salidroside might be a COX-2 inhibitor. Molecule modeling indicated that salidroside can directly bind with COX-2, which was proved by in vitro pull-down binding assay. Ex vivo studies showed that salidroside has no toxicity to cells, and inhibits the production of PGE2, phosphorylation of p38 or JNKs, and secretion of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) caused by SUV irradiation. In vivo studies demonstrated that salidroside attenuates the skin inflammation induced by SUV. In brief, our data provided the evidences for the protective role of salidroside against SUV-induced inflammation by targeting COX-2, and salidroside might be a promising drug for the treatment of SUV-induced skin inflammation.

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Section: Discussionmentioning

confidence: 99%

Salidroside suppresses solar ultraviolet-induced skin inflammation by targeting cyclooxygenase-2

Yuan

et al. 2016

Oncotarget

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“…For example, studies have reported that salidroside increases the neurological severity scores and reduces the cerebral edema and infarction volume at doses of 12 or 24 mg/kg (Zou YQ et al, 2009;Shi et al, 2012;Han, 2013). Our previous studies demonstrated that salidroside displayed strong and specific neuroprotective properties in MCAO-induced stroke with treatment (50 mg/kg, administered 1 h after the operation) once daily for 1, 2, and 6 days, or with only a two-time administration at a dose of 30 mg/kg (administered immediately before cerebral ischemia and after reperfusion) (Han et al, 2015;Lai et al, 2015;Lai et al, 2018). In a previous study, we found salidroside (30 mg/kg) reduced infarct size in 2,3,5-triphenyltetrazolium chloride-stained brain slices and improved histological changes in the cortex and striatum as revealed by Nissl staining (Han et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

“…Our previous studies demonstrated that salidroside displayed strong and specific neuroprotective properties in MCAO-induced stroke with treatment (50 mg/kg, administered 1 h after the operation) once daily for 1, 2, and 6 days, or with only a two-time administration at a dose of 30 mg/kg (administered immediately before cerebral ischemia and after reperfusion) (Han et al, 2015;Lai et al, 2015;Lai et al, 2018). In a previous study, we found salidroside (30 mg/kg) reduced infarct size in 2,3,5-triphenyltetrazolium chloride-stained brain slices and improved histological changes in the cortex and striatum as revealed by Nissl staining (Han et al, 2015). To further validate the effect of salidroside on cerebral ischemia/reperfusion, we used the balance beam test and foot fault test.…”

Section: Discussionmentioning

confidence: 99%

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Neuroprotective Effects of Salidroside on Cerebral Ischemia/Reperfusion-Induced Behavioral Impairment Involves the Dopaminergic System

et al. 2019

Self Cite

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Salidroside, a phenylpropanoid glycoside, is the main bioactive component of Rhodiola rosea L. Salidroside has prominent anti-stroke effects in cerebral ischemia/reperfusion models. However, the underlying mechanisms of its actions are poorly understood. This study examined the anti-stroke effects of salidroside in middle cerebral artery occlusion (MCAO)-induced rat model of stroke and its potential mechanisms involving the dopaminergic system. Salidroside administration increased the levels of dopamine (DA), homovanillic acid (HVA), and 3,4-dihydroxyphenylacetic acid (DOPAC) in the ipsilateral striatum after induction of transient ischemia, which were assessed using microdialysis with high-performance liquid chromatography coupled with electrochemical detection (HPLC-ECD). Furthermore, treatment with salidroside ameliorated neurobehavioral impairment, assessed with the modified neurological severity scores (mNSS), the balance beam test, and the foot fault test. Moreover, enzyme-linked immunosorbent assay (ELISA) suggested that MCAO-induced reduction in monoamine oxidase (MAO) was inhibited by salidroside. Immunohistochemical and immunofluorescence analyses revealed high level of tyrosine hydroxylase (TH) in the ipsilateral striatal caudate putamen (CPu) after cerebral ischemia/ reperfusion, which could be further elevated by salidroside. In addition, salidroside could reverse the decreased immunoreactivity of TH in the substantia nigra pars compacta (SNpc). These results suggest that the anti-stroke effects of salidroside in MCAO-induced cerebral ischemia/reperfusion may involve the modulation of monoamine metabolism in the striatum and SNpc, which may be related to the function of the dopaminergic system in the rat brain.

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“…It has been demonstrated that SAL is neuroprotective against ischemic cerebral injury, a leading cause of disability and mortality worldwide and is therefore considered to be a major public health problem ( 5 ). It has been demonstrated that SAL reduces the infarct volume and improves neurological deficit scores in a rat model of transient focal cerebral ischemia and reperfusion ( 6 ). In addition, SAL improves learning and spatial memory during hypoxia treatment, indicating that SAL has a neuroprotective effect during hypoxia ( 7 ).…”

Section: Introductionmentioning

confidence: 99%

Salidroside attenuates hypoxia/reoxygenation‑induced human brain vascular smooth muscle cell injury by activating the SIRT1/FOXO3α pathway

Jia

Wang

et al. 2017

Exp Ther Med

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It has been reported that salidroside (SAL), a natural dietary isothiocyanate, exhibits neuroprotective roles in cerebral ischemia-reperfusion injury. However, to the best of our knowledge, its underlying protective mechanism remains unknown. Sirtuin 1 (SIRT1) is a class III histone deacetylase involved in a variety of cellular functions. SIRT1 has been identified as a mediator of cerebral ischemia and may induce neuroprotection by activating various intracellular downstream targets, such as forkhead box protein O3α (FOXO3α). Therefore, the present study aimed to investigate whether SAL protects human brain vascular smooth muscle cells (HBVSMC) against hypoxia/reoxygenation (H/R) injury, which is a cell model of cerebral ischemia-reperfusion injury, through regulating the SIRT1-activited signaling pathway. The present study revealed that H/R treatment significantly reduced the expression of SIRT1 protein in HBVSMCs. Additionally, pretreatment with SAL reversed the H/R-induced decrease in cellular viability, increased caspase-3 activity, the appearance of apoptotic cells and the apoptosis rate in HBVSMCs. SAL attenuated the H/R-induced decrease in the expression of SIRT1 and phosphorylated FOXO3α protein in HBVSMCs, suggesting that the protective role of SAL in H/R injury occurs via the SIRT1/FOXO3α pathway. Furthermore, sirtinol, a SIRT1-specific inhibitor, suppressed the inhibitory effects of SAL on H/R-induced cytotoxicity and apoptosis as indicated by the downregulation of cell viability and upregulation of caspase-3 activity and apoptosis rate induced by sirtinol treatment in HBVSMCs. The reversal effects of SAL on H/R-induced alternation of B-cell lymphoma (Bcl-2) and Bcl-2 associated X protein expression were also attenuated by sirtinol. These results suggest that SAL exhibits neuroprotective effects against H/R injury by activating the SIRT1/FOXO3α pathway, which may become a novel potential therapeutic target for the treatment of cerebral ischemic disease.

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Neuroprotective effects of salidroside on focal cerebral ischemia/reperfusion injury involves the nuclear erythroid 2-related factor 2 pathway

Cited by 41 publications

References 28 publications

Salidroside suppresses solar ultraviolet-induced skin inflammation by targeting cyclooxygenase-2

Salidroside suppresses solar ultraviolet-induced skin inflammation by targeting cyclooxygenase-2

Neuroprotective Effects of Salidroside on Cerebral Ischemia/Reperfusion-Induced Behavioral Impairment Involves the Dopaminergic System

Salidroside attenuates hypoxia/reoxygenation‑induced human brain vascular smooth muscle cell injury by activating the SIRT1/FOXO3α pathway

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