Icariin protects cerebral neural cells from ischemia‑reperfusion injury in an <i>in vitro</i> model by lowering ROS production and intracellular calcium concentration

Ning, Ke; Gao, Rong

doi:10.3892/etm.2023.11849

Cited by 2 publications

(1 citation statement)

References 74 publications

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“…Subsequent blood reperfusion process will lead to massive production of ROS and further expand the damage. A previous study demonstrated that ICA protects cerebral neural cells from I/R injury by lowering ROS production and intracellular calcium concentration(Ning and Gao 2023 ). Here in, we established an in vitro oxidative damage model by treating PC-12 cells with 200µM H 2 O 2 for 8 h. After pre-treatment with ICT, the mortality rate of model cells was reduced, while the intracellular ROS level was significantly decreased, indicating that ICT is a potential therapeutic drug for alleviating oxidative damage.…”

Section: Discussionmentioning

confidence: 99%

Icariin improves oxidative stress injury during ischemic stroke via inhibiting mPTP opening

Zhou,

Li,

et al. 2024

Mol Med

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Background Ischemic stroke presents a significant threat to human health due to its high disability rate and mortality. Currently, the clinical treatment drug, rt-PA, has a narrow therapeutic window and carries a high risk of bleeding. There is an urgent need to find new effective therapeutic drugs for ischemic stroke. Icariin (ICA), a key ingredient in the traditional Chinese medicine Epimedium, undergoes metabolism in vivo to produce Icaritin (ICT). While ICA has been reported to inhibit neuronal apoptosis after cerebral ischemia-reperfusion (I/R), yet its underlying mechanism remains unclear. Methods PC-12 cells were treated with 200 µM H2O2 for 8 h to establish a vitro model of oxidative damage. After administration of ICT, cell viability was detected by Thiazolyl blue tetrazolium Bromide (MTT) assay, reactive oxygen species (ROS) and apoptosis level, mPTP status and mitochondrial membrane potential (MMP) were detected by flow cytometry and immunofluorescence. Apoptosis and mitochondrial permeability transition pore (mPTP) related proteins were assessed by Western blotting. Middle cerebral artery occlusion (MCAO) model was used to establish I/R injury in vivo. After the treatment of ICA, the neurological function was scored by ZeaLonga socres; the infarct volume was observed by 2,3,5-Triphenyltetrazolium chloride (TTC) staining; HE and Nissl staining were used to detect the pathological state of the ischemic cortex; the expression changes of mPTP and apoptosis related proteins were detected by Western blotting. Results In vitro: ICT effectively improved H2O2-induced oxidative injury through decreasing the ROS level, inhibiting mPTP opening and apoptosis. In addition, the protective effects of ICT were not enhanced when it was co-treated with mPTP inhibitor Cyclosporin A (CsA), but reversed when combined with mPTP activator Lonidamine (LND). In vivo: Rats after MCAO shown cortical infarct volume of 32–40%, severe neurological impairment, while mPTP opening and apoptosis were obviously increased. Those damage caused was improved by the administration of ICA and CsA. Conclusions ICA improves cerebral ischemia-reperfusion injury by inhibiting mPTP opening, making it a potential candidate drug for the treatment of ischemic stroke. Graphical Abstract

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Section: Discussionmentioning

confidence: 99%

Icariin improves oxidative stress injury during ischemic stroke via inhibiting mPTP opening

Zhou,

Li,

et al. 2024

Mol Med

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Hsa-miR-301a-3p inhibited the killing effect of natural killer cells on non-small cell lung cancer cells by regulating RUNX3

Zhang¹,

Yang²,

Wei³

et al. 2023

CBM

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BACKGROUND: Non-small cell lung cancer (NSCLC) is the most commonly diagnosed solid tumor. Natural killer (NK) cell-based immunotherapy is a promising anti-tumor strategy in various cancers including NSCLC. OBJECTIVE: We aimed to investigate the specific mechanisms that regulate the killing effect of NK cells to NSCLC cells. METHODS: Reverse transcription-quantitative PCR (RT-qPCR) assay was applied to measure the levels of hsa-microRNA (miR)-301a-3p and Runt-related transcription factor 3 (RUNX3). Enzyme-linked immunosorbent assay (ELISA) was used to measure the levels of IFN-γ and TNF-α. Lactate dehydrogenase assay was applied to detect the killing effect of NK cells. Dualluciferase reporter assay and RNA immunoprecipitation (RIP) assay were carried out to confirm the regulatory relationship between hsa-miR-301a-3p and RUNX3. RESULTS: A low expression of hsa-miR-301a-3p was observed in NK cells stimulated by IL-2. The levels of IFN-γ and TNF-α were increased in NK cells of the IL-2 group. Overexpression of hsa-miR-301a-3p reduced the levels of IFN-γ and TNF-α as well as the killing effect of NK cells. Furthermore, RUNX3 was identified to be a target of hsamiR-301a-3p. hsa-miR-301a-3p suppressed the cytotoxicity of NK cells to NSCLC cells by inhibiting the expression of RUNX3. We found hsa-miR-301a-3p promoted tumor growth by suppressing the killing effect of NK cells against NSCLC cells in vivo. CONCLUSIONS: Hsa-miR-301a-3p suppressed the killing effect of NK cells on NSCLC cells by targeting RUNX3, which may provide promising strategies for NK cell-based antitumor therapies.

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Icariin protects cerebral neural cells from ischemia‑reperfusion injury in an in vitro model by lowering ROS production and intracellular calcium concentration

Cited by 2 publications

References 74 publications

Icariin improves oxidative stress injury during ischemic stroke via inhibiting mPTP opening

Icariin improves oxidative stress injury during ischemic stroke via inhibiting mPTP opening

Hsa-miR-301a-3p inhibited the killing effect of natural killer cells on non-small cell lung cancer cells by regulating RUNX3

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