To explore the potential mechanism of cinnamaldehyde in alleviating nerve injury in rats with traumatic brain injury (TBI).

Rats were randomly divided into sham group (only craniotomy), model group(TBI model), experimental-L group (TBI+25 mg·kg^-1 cinnamaldehyde), experimental-H group (TBI+75 mg·kg^-1 cinnamaldehyde), miR-NC group (TBI+miR-NC lentivirus+75 mg·kg^-1 cinnamaldehyde) and miR-27a-3p inhibitor group (TBI+miR-27a-3p inhibitor lentivirus+75 mg·kg^-1 cinnamaldehyde). After treatment, real-time quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression of miR-27a-3p; the Morris water maze test was used to assess memory function; immunofluorescence assay was used to detect the expression of ionized calcium-binding adapter molecule 1 (Iba-1); Western blot was used to detect the expression of related proteins in brain tissues; and the dual-luciferase reporter gene assay was used to verify the binding of miR-27a-3p to BCL2/adenovirus E1B 19kDa interacting protein 3-like (BNIP3L).

The relative expression levels of miR-27a-3p in the sham group, model group, experimental-L group, experimental-H group, miR-NC group and miR-27a-3p inhibitor group were 1.00±0.08, 0.40±0.03, 0.52±0.08, 0.76±0.08, 0.73±0.09 and 0.18±0.02, respectively; the escape latency times were (11.19±0.75), (26.06±1.47), (23.59±1.39), (14.95±1.71), (15.37±0.77) and (24.91±1.96) s, respectively; the Iba-1 fluorescence intensities were (1 189.50±113.68), (2 958.70±279.29), (2 287.05±271.69), (1 916.55±205.44), (1 935.57±164.54) and (2 564.52±333.05) a.u., respectively; the relative expression levels of autophagy-related gene 5 (ATG5) protein were 0.32±0.03, 0.94±0.07, 0.71±0.09, 0.50±0.08, 0.53±0.07 and 0.85±0.09, respectively; the relative expression levels of Beclin-1 autophagy regulator (Beclin-1) protein were 0.35±0.03, 0.95±0.13, 0.75±0.12, 0.49±0.05, 0.48±0.07 and 0.73±0.10, respectively; the relative expression levels of Parkin RBR domain E3 ubiquitin protein ligase (Parkin) protein were 0.29±0.04, 0.64±0.08, 0.51±0.09, 0.41±0.04, 0.43±0.05 and 0.62±0.07, respectively. For the above indicators, there were all statistically significant differences when comparing the model group with the sham group, the experimental-L and experimental-H groups with the model group, and the miR-27a-3p inhibitor group with the miR-NC group (P<0.05, P<0.01, P<0.001). The dual-luciferase reporter gene assay confirmed the targeted binding of miR-27a-3p to BNIP3L.

Cinnamaldehyde may regulate autophagy through the miR-27a-3p/BNIP3L axis, improve neurological function, alleviate neuroinflammation and exert neuroprotective effects on TBI-induced brain injury.