Lycopene protects against early brain injury after subarachnoid hemorrhage via suppressing endoplasmic reticulum stress.

OBJECTIVES

Neuroinflammation is closely associated with the poor prognosis of patients with subarachnoid hemorrhage (SAH). Lycopene (Lyc), a naturally occurring carotenoid, possesses multiple pharmacological effects, especially its neuroprotective function. However, the role of Lyc in SAH has never been evaluated.

METHODS

In this study, the C57BL/6 mouse SAH model was induced by the endovascular perforation method. Lyc was administered to the mice intragastrically, and tunicamycin, an endoplasmic reticulum stress (ERS) agonist, was injected intravenously. The effects of Lyc on early brain injury (EBI) were assessed using neurological scoring, hematoxylin and eosin staining, and Nissl staining. Western blotting was used to analyze ERS-related proteins. Immunofluorescence staining was used to analyze microglial cell activation.

RESULTS

Lyc significantly improved the neurobehavioral scores and alleviated neuronal degeneration at 24 h after SAH. Moreover, Lyc significantly reduced the expression levels of proteins p-eIF2a/eIF2a, ATF4, and CHOP and decreased the activation of microglial cells. Furthermore, tunicamycin reversed the inhibitory effect of Lyc on ERS and microglial cell activation, accompanied by improvement in neurological function.

CONCLUSION

Lyc relieved SAH-induced EBI partly through the p-eIF2a/ATF4/CHOP pathway.