Journal
PHYTOMEDICINE
Volume 90, Issue -, Pages -Publisher
ELSEVIER GMBH
DOI: 10.1016/j.phymed.2021.153630
Keywords
Intracerebral hemorrhage; NR2B/p38 signals pathway; Da-cheng-qi decoction; Emodin
Categories
Funding
- National Natural Science Foundation of China [91539112]
- Health Committee of Hubei Province [ZY2021M041]
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The study confirmed the protective effects of DCQ on ICH, possibly through the inhibition of MAPK and activation of M2 microglia. These results are beneficial for the development of therapeutic targets for ICH.
Background: Intracerebral hemorrhage (ICH), the most fatal subtype of stroke, has no disease-modifying treatment. Da-cheng-qi decoction (DCQ), composed of rhubarb, is one of the most commonly used Chinese traditional decoctions in ICH treatment. But the mechanism is not clear. Emodin is an active compound found in rhubarb. Purpose: To study the protective effects of DCQ on ICH and its possible mechanisms of action. Methods: The ICH model was reproduced by injecting collagenase-VII into the left caudate putamen (CPu) of rats. DCQ and emodin were used to treat the ICH rats for 7 days. Behavior tests, proteomic analysis, morphological studies, and western blotting were performed. Results: The neurological deficits in the ICH rats recovered with DCQ and emodin on the 14th day after ICH. The proteomics data revealed that DCQ significantly corrected the pathological signals in the CPu and hippocampus after ICH. The numbers of amoebic microglia in the CPu and M2 microglia in both CPu and hippocampus were significantly increased after DCQ and emodin treatment. The increase in GluN2B-containing NMDA receptor (NR2B) and postsynaptic density protein-95, activation of mitogen-activated protein kinase (MAPK) signals in the CPu, and secondary neurodegeneration (SND) in the hippocampus were significantly recovered in DCQ-treated rats. Inhibition of MAPK p38 (p38) in the hippocampus was observed after DCQ and emodin treatment. Conclusion: The protective effects of DCQ on ICH were confirmed in this study, and its mechanism may be related to the inhibition of MAPK and activation of M2 microglia. These results are beneficial to the development of ICH therapeutic targets.
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