Crocetin protects mouse brain from apoptosis in traumatic brain injury model through activation of autophagy

ABSTRACT

Background

Autophagy is recognized as a promising therapeutic target for traumatic brain injury (TBI). Crocetin is an aglycone of crocin naturally occurring in saffron and has been found to alleviate brain injury diseases. However, whether crocetin affects autophagy after TBI remains unknown. Therefore, we explore crocetin roles in autophagy after TBI.

Methods

We used a weight-dropped model to induce TBI in C57BL/6J mice. Neurological severity scoring (NSS) and grip tests were used to evaluate the neurological level of injury. Brain edema, neuronal apoptosis, neuroinflammation and autophagy were detected by measurements of brain water content, TUNEL staining, ELISA kits and western blotting.

Results

Crocetin ameliorated neurological dysfunctions and brain edema after TBI. Crocetin reduced neuronal apoptosis and neuroinflammation and enhanced autophagy after TBI.

Conclusion

Crocetin alleviates TBI by inhibiting neuronal apoptosis and neuroinflammation and activating autophagy.

KEYWORDS:

• Traumatic brain injury
• crocetin
• autophagy
• apoptosis
• neuroinflammation

Acknowledgments

The authors appreciate the help of Wuhan Caidian District People’s Hospital.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Additional information

Funding

The author(s) reported there is no funding associated with the work featured in this article.