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Neuroinflammation accompanied by microglial activation triggers multiple cell death after traumatic brain injury (TBI). The secondary injury caused by inflammation may persist for a long time. Recently, platelet C‐type lectin‐like 2 receptor (CLEC‐2) has been shown to regulate inflammation in certain diseases. However, its possible effects on TBI remain poorly understood. Here, we aimed to investigate...
Cognitive impairment is one of the most common and devastating neuropsychiatric sequelae after traumatic brain injury (TBI), and hippocampal neuronal survival plays a causal role in this pathological process. Resolvin D1 (RvD1), an important endogenous specialized pro‐resolving mediator, has recently been reported to exert a potent protective effect on mitochondria. This suggests that RvD1 may suppress...
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