Chrysotoxine attenuates sevoﬂurane-induced neurotoxicity in vitro via regulating PI3K/AKT/GSK pathway

doi:10.22514/sv.2021.107

Cited by 8 publications

(6 citation statements)

References 23 publications

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“…SEV was able to relieve LPS-induced apoptosis and oxidative stress to protected HK-2 cells by inactivating NF- κ B signaling [ 8 ]. SEV can also promote the apoptosis of neural stem cells and inhibit their proliferation [ 9 ] by disrupting their differentiation ability [ 10 ].…”

Section: Introductionmentioning

confidence: 99%

MFG-E8 Exerts Neuroprotection in Neural Stem Cells Induced by Anesthetic Sevoflurane via Regulating the PI3K/AKT Pathways

Cai

Sheng

2022

Stem Cells International

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MFG-E8 has shown tissue protection effects in various models of organ injury. In this study, the function of MFG-E8 in SEV-induced neural stem cells (NSCs) was studied. The cell viability and apoptosis affected by rhMFG-E8 were tested by MTT and flow cytometry analysis, respectively. Then, the mRNA expression of MFG-E8 was detected by qRT-PCR. The expression of SOD, GSF-Px, and MDA was assessed using ELISA assay. Western blot analysis was applied for assessing the expression of MFG-E8, BCL2, BAX, cleaved caspase-3, GRP-78, XBP-1, ATF-6, ATF-4, CHOP, p-PI3K, PI3K, p-AKT, and AKT. The pharmacological experiments suggested that both mRNA and protein expression of MFG-E8 were significantly decreased after 24 h, 48 h, and 72 h treatment with SEV, and the Western blot results displayed that 50 and 100 μg/ml rhMFG-E8 could evidently promote the expression of MFG-E8 in NSCs induced by SEV. Next, rhMFG-E8 reduced the apoptosis of NSCs induced by SEV through upregulating Bcl-2 and cleaved caspase-3 and downregulating Bax. Moreover, rhMFG-E8 alleviated the endoplasmic reticulum pressure of NSCs induced by SEV through decreasing the expression of GRP-78, XBP-1, ATF-6, ATF-4, and CHOP. In addition, the rhMFG-E8 could promote the expression of SOD and GSH-Px and inhibit the expression of MDA and LDH detected by the ELISA assay and LDH kit. Moreover, rhMFG-E8 elevated the expression of p-PI3K/PI3K and p-AKT/AKT, which were inhibited by SEV in NSCs. The results of this project supported that rhMFG-E8 protects neural activity in neural stem cells induced by anesthetic sevoflurane via regulating the PI3K/AKT pathways.

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Section: Introductionmentioning

confidence: 99%

MFG-E8 Exerts Neuroprotection in Neural Stem Cells Induced by Anesthetic Sevoflurane via Regulating the PI3K/AKT Pathways

Cai

Sheng

2022

Stem Cells International

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“…Alteration in the expression of microRNAs, tamoxifen metabolism, and modification in the PI3K cell survival pathway contribute to resistance of BC to tamoxifen [14,15]. Moreover, ERK signaling is associated with tamoxifenresistance of BC through regulation of cell apoptotic pathway [16].…”

Section: Discussionmentioning

confidence: 99%

Knockdown of FK506-binding proteins 14 enhances tamoxifen-sensitivity of breast cancer through PI3K/AKT and ERK signaling

Ma¹,

Zhao²,

Gong³

et al. 2023

Trop. J. Pharm Res

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Purpose: To investigate the effect of FK506-binding proteins 14 (FKBP14) in the development of chemoresistance of breast cancer. Methods: Breast cancer cell lines (MCF-7 and T47D) were exposed to 4-hydroxytamoxifen over a long period to establish tamoxifen-resistant (TamR) cells. Cell proliferation was evaluated by MTT and colony formation assays, while Transwell assay was used to investigate cell migration and invasion. Results: TamR cells showed resistance to 4-hydroxytamoxifen through increase in IC50 for 4-hydroxytamoxifen in MCF-7 and T47D. The FKBP14 was significantly up-regulated in TamR cells (p < 0.05). Knockdown of FKBP14 reduced the IC50 for 4-hydroxytamoxifen in TamR cells. The number of colony formation in TamR cells was also significantly decreased by silencing of FKBP14 (p < 0.01). Knockdown of FKBP14 inhibited the migration and invasion of TamR cells. Protein expression of p-AKT, p-PI3K and p-ERK in TamR cells were down-regulated by silencing of FKBP14. Conclusion: Loss of FKBP14 enhances sensitivity to tamoxifen in TamR MCF-7 and T47D cells through inactivation of PI3K/AKT and ERK signaling. The role of FKBP14 in tamoxifen-resistant animal models needs further investigation.

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“…Interference of Bcl-3 reduced p-Akt and p-GSK3β Akt/GSK3β signaling plays a critical role in cell apoptosis, proliferation, and survival. 25 Activation of PI3K/Akt/ mechanistic target of rapamycin (mTOR) up-regulated expression of IL-17A, TNF-α, and IL-1β, and contributed to the development of psoriasis. 26 Inhibition of PI3K/Akt/ mTOR attenuated psoriasis 27 and psoriasis with dyslipidemia.…”

Section: Knockdown Of Bcl-3 Mediated Akt/gsk3β Signaling In Imiquimod...mentioning

confidence: 99%

Knockdown of Bcl-3 alleviates psoriasis and dyslipidemia comorbidity by regulating Akt pathway

Yang²,

Chao³

2022

Allergol Immunopathol

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Background: Psoriasis is considered as an inflammatory skin disease accompanied by dyslipid-emia comorbidity. B-cell leukemia-3 (Bcl-3) belongs to IκB (inhibitor of nuclear factor kappa B [NF-κB]) family, and regulates inflammatory response through associating with NF-κB. The role of Bcl-3 in psoriasis was investigated in this study. Methods: Apolipoprotein E (ApoE)-deficient mice were treated with imiquimod to induce psoriasis and dyslipidemia. Mice were injected intradermally in the back with lentiviral particles encoding Bcl-3 small hairpin RNA (shRNA). Hematoxylin and eosin were used to detect pathological characteristics. The blood lipid levels were determined by automatic biochemical analyzer, and inflammation was assessed by enzyme-linked-immunosorbent serologic assay and real-time quantitative reverse transcription polymerase chain reaction. Results: Bcl-3 was elevated in imiquimod-induced ApoE-deficient mice. Injection with lentiviral particles encoding Bcl-3 shRNA reduced Psoriasis area and severity index (PASI) score in ApoE-deficient psoriatic mice. Knockdown of Bcl-3 also ameliorated imiquimod-induced psoriasiform skin lesions in ApoE-deficient mice. Moreover, loss of Bcl-3 enhanced expression of loricrin, an epidermal barrier protein, reduced expression of proliferating cell nuclear antigen (PCNA) and lectin-like oxidized LDL (oxLDL) receptor-1 (LOX-1) in imiquimod-induced ApoE-deficient mice. The enhanced levels of blood lipid in ApoE-deficient mice were attenuated by silencing of Bcl-3 with increase of high-density lipoprotein, and reduction of total cholesterol, triglycerides, and low-density lipoprotein cholesterol. Knockdown of Bcl-3 attenuated imiquimod-induced decrease of transforming growth factor beta (TGF-β), and increase of Interleukin (IL)-17A, IL-23, IL-6, and tumor necrosis factor-α (TNF-α) in ApoE-deficient mice. Protein expression of phospho-Akt (p-Akt) and p-GSK3β in ApoE-deficient psoriatic mice was decreased by silencing of Bcl-3. Conclusion: Loss of Bcl-3 exerted anti-inflammatory effect on psoriasis and dyslipidemia comorbidity through inactivation of Akt/GSK3β pathway.

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Chrysotoxine attenuates sevoﬂurane-induced neurotoxicity in vitro via regulating PI3K/AKT/GSK pathway

Cited by 8 publications

References 23 publications

MFG-E8 Exerts Neuroprotection in Neural Stem Cells Induced by Anesthetic Sevoflurane via Regulating the PI3K/AKT Pathways

MFG-E8 Exerts Neuroprotection in Neural Stem Cells Induced by Anesthetic Sevoflurane via Regulating the PI3K/AKT Pathways

Knockdown of FK506-binding proteins 14 enhances tamoxifen-sensitivity of breast cancer through PI3K/AKT and ERK signaling

Knockdown of Bcl-3 alleviates psoriasis and dyslipidemia comorbidity by regulating Akt pathway

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