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Fig. 8 | Journal of Neuroinflammation

Fig. 8

From: EETs/sEHi alleviates nociception by blocking the crosslink between endoplasmic reticulum stress and neuroinflammation in a central poststroke pain model

Fig. 8

Schematic diagram showing the involvement of EETs/sEHi in modulating the crosslink between ER stress and neuroinflammation under stroke and the subsequent CPSP condition. Stroke activates the ER stress response (UPR) to protect cells against toxic accumulation of misfolded proteins, as well as help maintain the functional integrity of ER. However, prolonged UPR instructs the stressed neurons to commit suicide by triggering apoptosis, which elicits a defensive innate immune response against the invading pathogens that cause glial cell activation and excessive neuroinflammation. The excessive neuroinflammation, in turn, exacerbates ER stress. The vicious interactions between ER stress and neuroinflammation result in central sensitization and pain and deleteriously contribute to stroke damage, the suppression of which by sEHi/EETs may provide a therapeutic approach for stroke and CPSP

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