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The effect of oridonin regulating the IL-6/STAT3 signaling pathway on proliferation,autophagy, apoptosis,and inflammatory response in microglia subjected to oxygen-glucose deprivation/reoxygenation
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DOI   10.11656/j.issn.1673-9043.2026.03.07
Key Words   oridonin;IL-6/STAT3 signaling pathway;oxygen-glucose deprivation/reoxygenation;microglia;proliferation;autophagy;apoptosis
Author NameAffiliationE-mail
LI Lin Department of Neurosurgery, North China University of Technology Affiliated Hospital, Tangshan 063015, China  
LI Xiangnan Department of Neurosurgery, North China University of Technology Affiliated Hospital, Tangshan 063015, China  
YANG Songtao Department of Neurosurgery, North China University of Technology Affiliated Hospital, Tangshan 063015, China  
LI Jianmin Department of Neurosurgery, North China University of Technology Affiliated Hospital, Tangshan 063015, China  
ZHANG Yunhe Department of Neurosurgery, North China University of Technology Affiliated Hospital, Tangshan 063015, China  
FU Aijun Department of Neurosurgery, North China University of Technology Affiliated Hospital, Tangshan 063015, China  
ZHANG Zhiyong Department of Neurosurgery, North China University of Technology Affiliated Hospital, Tangshan 063015, China zzy1895@126.com 
Abstract
    [Objective] To investigate the effect of oridonin(ORI) on proliferation,autophagy,apoptosis,and inflammatory response in microglia subjected to oxygen-glucose deprivation/reoxygenation(OGD/R) and its potential mechanism involving the interleukin-6(IL-6)/signal transducer and activator of transcription 3(STAT3) signaling pathway. [Methods] BV2 microglial cells were divided into the following groups:control,OGD/R,ORI(low,medium,and high concentration:ORI-L,ORI-M,ORI-H),and ORI combined with recombinant IL-6. After respective treatments for 24 h,cell proliferation was assessed by Cell Counting Kit-8(CCK-8) assay and 5-ethynyl-2'-deoxyuridine(EdU) staining. Autophagy was observed under a transmission electron microscope. Apoptosis was detected by flow cytometry. The levels of inflammatory factors [tumor necrosis factor-α(TNF-α),IL-18,and IL-1β] were measured using enzyme-linked immunosorbent assay(ELISA). The protein expression levels of IL-6 and STAT3 were determined by Western blotting. [Results] Compared with the control group,the OGD/R group showed decreased cell viability and EdU-positive cell rate,along with increased number of autophagic vacuoles,apoptosis rate,levels of TNF-α,IL-18,IL-1β,and protein expression of IL-6 and STAT3(P<0.01). Compared with the OGD/R group,the ORI-L,ORI-M,and ORI-H groups exhibited a concentration-dependent increase in cell viability and EdU-positive cell rate,and a concentration-dependent decrease in the number of autophagic vacuoles,apoptosis rate,levels of TNF-α,IL-18,IL-1β,and protein expression of IL-6 and STAT3(P<0.05). Compared with the ORI-H group,the ORI combined with recombinant IL-6 group demonstrated decreased cell viability and EdU-positive cell rate,and increased number of autophagic vacuoles,apoptosis rate,levels of TNF-α,IL-18,IL-1β,and protein expression of IL-6 and STAT3(P<0.01). [Conclusion] ORI can promote proliferation and inhibit autophagy,apoptosis,and inflammatory response in OGD/R-induced microglia. Its mechanism may be associated with the inhibition of the IL-6/STAT3 signaling pathway.

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