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Peripheral nerve injury is a common clinical issue induced by trauma, tumor, and damage caused by treatment. Such factors create chemical and inflammatory alterations at the injury site, which increase nerve deterioration. Thus, minimizing these modifications can lead to nerve protection after injury. The present study sought to evaluate the possible improvement in nerve regeneration and enhancement of functional outcomes by cinnamaldehyde (Cin) administration following sciatic nerve crush in a rat model. Rats (n = 48) were distributed into 6 groups, including sham, injury, DMSO (vehicle group), and Cin groups (10, 30, and 90 mg/kg/day). Using small hemostatic forceps, crush injury was induced in the left sciatic nerve. Thereafter, Cin was administered for 28 successive days. Weekly records were taken for sciatic functional index (SFI) measurements. Further assessments including electrophysiological and histomorphometric evaluations, gastrocnemius muscle wet weight measurements, and estimation of the serum total oxidant status were performed. According to the results, Cin could accelerate sciatic nerve recovery after crush injury, and the dose of 30 mg/kg/day of Cin had better impacts on SFI recovery, muscle mass ratio, and myelin content. The current research demonstrated that Cin positively affects peripheral nerve restoration. Therefore, Cin therapy could be considered as a potential treatment method for peripheral nerve regeneration and its functional recovery. However, more investigations are required to further validate the study results and evaluate the optimal dose of Cin.