l-Theanine alleviates the neuropathological changes induced by PCB (Aroclor 1254) via inhibiting upregulation of inflammatory cytokines and oxidative stress in rat brain

- Aroclor 1254 caused impairment in motor and cognitive performance.
- Neuronal loss was observed in cerebral cortex, hippocampus and cerebellum.
- Inflammatory cytokines were upregulated in aroclor 1254 induced rats.
- l-Theanine significantly improved the neurobehavioral activities.
- It also reduced the abnormal expression of inflammatory cytokines.

The present study is aimed at evaluating the protective role of l-theanine on aroclor 1254-induced oxidative stress in rat brain. Intraperitoneal administration of Aroclor 1254 (2 mg/kg b.wt. for 30 days) caused oxidative stress in rat brain and also caused neurobehavioral changes. Oxidative stress was assessed by determining the levels of lipid peroxide (LPO), protein carbonyl content, and changes in activities of creatine kinase (CK), acetylcholinesterase (AchE), and ATPases in the hippocampus, cerebellum and cerebral cortex of control and experimental rats. Histopathological results showed that PCB caused neuronal loss in all three regions. PCB upregulated the mRNA expressions of inflammatory cytokines. Oral administration of l-theanine (200 mg/kg b.wt.) increased the status of antioxidants, decreased the levels of LPO, nitric oxide (NO) and increased the activities of CK, AchE and ATPases. l-Theanine restored normal architecture of brain regions and downregulated the expression of inflammatory cytokines. In conclusion, l-theanine shows a protective role against PCBs-induced oxidative damage in rat brain.