Baicalin is known to exhibit neuroprotective effects during brain injury through its antioxidant and anti-inflammatory functions. Moreover, γ-enolase is specifically expressed in nerve cells and exhibits neuroprotective properties. In this study, we investigated whether baicalin regulates γ-enolase expression in an moddle cerebral artery occulsion (MCAO)-induced brain injury model. Adult male rats were intraperitoneally injected with baicalin (100 mg/kg) or phosphate-buffered saline (PBS) immediately after right MCAO surgery. Neurological behavior tests were performed 24 hours after surgery and brain water content was evaluated. Right cortical tissue was collected. Western blot analysis were conducted to elucidate γ-enolase expression in MCAO animals treated with baicalin. In addition, γ-enolase expression was analyzed using immunofluorescence staining. MCAO animals administered PBS displayed severe behavioral impairments and edema, whereas baicalin administration alleviated these disorders, demonstrating the protective effects of baicalin against ischemic damage. Western blot analysis results showed that MCAO-induced damage decreased γ-enolase expression, and baicalin treatment mitigated this reduction. These findings were confirmed through immunofluorescence staining. Since γ-enolase is known to contribute to neuroprotective effects, these results suggest that baicalin alleviates neurobehavioral impairments in stroke animals and exerts neuroprotective effects by attenuating the decline in γ-enolase expression caused by brain injury. In conclusion, we demonstrated that baicalin regulates γ-enolase expression during cerebral ischemic damage.

Ischemic stroke is caused by a blockage of the cerebral artery, which leads to a severe neurological disorder. Chlorogenic acid is a phenolic acid found mainly in plants such as coffee beans, eggplants, and carrots. It exerts a neuroprotective effect against cerebral ischemic damage. Bcl-2 family protein is a representative apoptosis regulatory protein. Bcl-2 and Bcl-xL act as apoptosis inhibitors, while Bax and Bad act as apoptosis inducers.The interaction of Bcl-2 family protein plays an important role in determining cell fate. The aim of this study was to investigate whether chlorogenic acid modulates the interaction of Bcl-2 family proteins during ischemic injury. Middle cerebral artery occlusion (MCAO) surgery was performed to induce cerebral ischemia. Chlorogenic acid (30 mg/kg) or phosphate buffered saline was intraperitoneally injected to adult male rats 2 h after MCAO surgery. Neurobehavioral tests were performed to confirm the neuroprotective effect of chlorogenic acid 24 h after MCAO injury, and immunoprecipitation analysis was performed to investigate the interaction of Bcl-2 family protein. MCAO damage showed signs of severe neurological disorders, while chlorogenic acid improved these disorders. Results of immunoprecipitation analysis were as follows. Interaction between Bax and Bcl-2 or Bcl-xL was decreased in MCAO injury, chlorogenic acid prevents these decreases. In contrast to Bax, Interaction between Bad and Bcl-2 or Bcl-xL was increased in MCAO injury, chlorogenic acid prevents these increases. Furthermore, chlorogenic acid attenuated MCAO-induced increase of capase-9. In conclusion, our findings demonstrate that chlorogenic acid exerts a neuroprotective effect against cerebral ischemic injury by modulating interaction of Bcl-2 family proteins.

Stroke occurs when local thrombosis, embolic particle or the rupture of blood vessele interrupts the blood floe to the brain. -estradiol 17-valerate has been reported to exert neuroprotective effects when administered before an ischemic insult. Recently, the pathophysiology of cerebral ischemia has been studied extensively in rat with various methods. In the present study, we investigates whether -estrodiol 17-valerate can protect against brain injury. RNA sample were extracted from the hippocampus of female rat, reverse-transcription in the presence of [32p] dATP. Differential gene express-ion profiles were revealed (Bone morphogenetic protein type 1A receptor, Protein disulphide isomerase, Leukemia inhibitor factor receptor, cytochrome bc- 1 complex-x core P, thiol-specific antioxidant protein). RT-PCR was used to validate the relative expression pattern obtained by the cDNA array. The precise relationship between the early expression of recovery genes and stroke is a matter of luther investigation. This Study was supported by the Korea Science and Engineering Foundation(KOSEF) through the Biohealth Products Research Center(BPRC), Inje University, Korea.