Phytomedicine : international journal of phytotherapy and phytopharmacology · 2024
Exploring the mechanism of Taohong Siwu Decoction in treating ischemic stroke injury via the circDnajc1/miR-27a-5p/C1qc signaling axis.
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Li Yumeng, Ye Qingping, Li Jingjing, Zhang Lijuan, Yu Chao, Xue Sujun, Li Shuangping, Duan Xianchun, Peng Daiyin
Аннотация
BACKGROUND: Ischemic stroke (IS) is the most prevalent type of cerebrovascular disease. Taohong Siwu Decoction (THSWD) has been demonstrated to have neuroprotective benefits during Cerebral Ischemia-Reperfusion Injury (CIRI). Whether THSWD mitigates CIRI by modulating the circDnajc1/miR-27a-5p/C1qc signaling axis is not known.
OBJECTIVE: Examine how THSWD provides neuroprotective benefits in reducing the damage wrought by IS.
METHODS: We employed middle cerebral artery occlusion/reperfusion (MCAO/R) rat model and oxygen glucose deprivation/re-oxygenation (OGD/R) in vitro model. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR), Western blot (WB), and immunofluorescence analyses (IF) were utilized to detect microglial activation markers TMEM119, CD11b, and Iba1, inflammatory mediators CCL2, CCL6, IL1, IL6, IL10, and TNF-α, as well as circDnajc1, miR-27a-5p, C1qc, C3, and C5aR.
CONCLUSION: Our data suggest that THSWD can mitigate inflammatory response, inhibit microglial activation and neuron apoptosis, and exert neuroprotective effects by regulating the circDnajc1/miR-27a-5p/C1qc signaling axis.
OBJECTIVE: Examine how THSWD provides neuroprotective benefits in reducing the damage wrought by IS.
METHODS: We employed middle cerebral artery occlusion/reperfusion (MCAO/R) rat model and oxygen glucose deprivation/re-oxygenation (OGD/R) in vitro model. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR), Western blot (WB), and immunofluorescence analyses (IF) were utilized to detect microglial activation markers TMEM119, CD11b, and Iba1, inflammatory mediators CCL2, CCL6, IL1, IL6, IL10, and TNF-α, as well as circDnajc1, miR-27a-5p, C1qc, C3, and C5aR.
CONCLUSION: Our data suggest that THSWD can mitigate inflammatory response, inhibit microglial activation and neuron apoptosis, and exert neuroprotective effects by regulating the circDnajc1/miR-27a-5p/C1qc signaling axis.