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Updated: Aug 2, 2026
Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
Published on: January 30, 2014
Baicalin-Geniposide combination modulates microglia polarization against chronic cerebral ischemia and concomitant
Tian Hu1, Qianqian Sun2, Jiahao Zhang2
1Pharmacology of Chinese medicine, Shaanxi University of Chinese Medicine, Xianyang 712046, China; Key Laboratory of Pharmacodynamics and Material Basis of Chinese Medicine of Shaanxi Administration of Traditional Chinese Medicine, Xianyang 712046, China; Engineering Research Center of Brain Health Industry of Chinese Medicine, Universities of Shaanxi Province, Xianyang 712046, China.
Background:
Baicalin and geniposide combination (BC/GD), a traditional Chinese medicine pairing, is beneficial for chronic cerebral ischemia (CCI) and kidney injury, but the underlying mechanism remains unknown.
Methods:
Using network pharmacology, we identified targets and pathways of BC/GD in CCI and kidney injury. Using molecular docking, we discovered the affinity between BC/GD and the key targets HIF-1α, EPOR, and TNF-α. Then, these were verified in SD rats and transwell co-cultures of HMC3 and HK-2 cells.
Results:
Experimental validation demonstrated that BC/GD ameliorated cerebral and kidney pathological injury, cognitive impairment, and kidney dysfunction, increased cerebral blood flow, inhibited microglia activation and polarization of pro-inflammatory phenotypes, increased the expression of HIF-1α and EPOR, and reduced the phosphorylation of NF-κB and the level of pro-inflammatory factors in CCI rats. Then, in vitro validation experiments, we found that 12.5 μM and 25 μM BC/GD significantly increased the levels of anti-inflammatory factors and modulated the HIF-1α/EPO/NF-κB pathway in oxygen-glucose-deprived HMC3 and HK-2 cells, which was partially antagonized by PX-478, an inhibitor of HIF-1α.
Conclusion:
BC/GD alleviated cerebral and kidney inflammatory injury, and its mechanism may be related to the modulation of microglia polarization through HIF-1α/EPO/NF-κB.
