Regulation of Bcl-2 Family Protein Changes by Chlorogenic Acid Treatment in Focal Cerebral Ischemia of Rats
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Ischemic stroke is a high mortality disease that causes irreversible damage. Chlorogenic acid is a polyphenolic substance withneuroprotective properties. Bcl-2 family proteins perform a critical role in apoptosis process. Bcl-2 and Bcl-xL are anti-apoptotic proteinsthat prevent cell death, and Bax and Bad are pro-apoptotic proteins that promote apoptosis. We investigated whether chlorogenic acidmodulates Bcl-2 family proteins during focal cerebral ischemia. We made a rat model of ischemic stroke by performing middle cerebralartery occlusion (MCAO). Chlorogenic acid (30 mg/kg) or phosphate-buffered saline was treated via intraperitoneal injection 2 hr beforeMCAO. Neurological behavioral tests were performed 24 hr after MCAO damage and cortical tissues were collected. Reversetranscription-PCR, Western blot, and immunofluorescence staining were performed to observe changes in Bcl-2 family proteins expression. MCAO-damage induced neurobehavioral disorders and chlorogenic acid alleviate these deficits. Bcl-2 and Bcl-xL expressions weredecreased and Bax and Bad expressions were increased in MCAO animals. However, chlorogenic acid treatment attenuated the decreaseof Bcl-2 and Bcl-xL and the increase of Bad and Bax due to MCAO surgery. Moreover, chlorogenic acid treatment attenuatedMCAO-induced upregulation of caspase-3. These findings suggest that chlorogenic acid exerts neuroprotective effects against MCAOdamage by regulating Bcl-2 family proteins including Bcl-2, Bcl-xL, Bax, and Bad.
Abstract
Ischemic stroke is a high mortality disease that causes irreversible damage. Chlorogenic acid is a polyphenolic substance withneuroprotective properties. Bcl-2 family proteins perform a critical role in apoptosis process. Bcl-2 and Bcl-xL are anti-apoptotic proteinsthat prevent cell death, and Bax and Bad are pro-apoptotic proteins that promote apoptosis. We investigated whether chlorogenic acidmodulates Bcl-2 family proteins during focal cerebral ischemia. We made a rat model of ischemic stroke by performing middle cerebralartery occlusion (MCAO). Chlorogenic acid (30 mg/kg) or phosphate-buffered saline was treated via intraperitoneal injection 2 hr beforeMCAO. Neurological behavioral tests were performed 24 hr after MCAO damage and cortical tissues were collected. Reversetranscription-PCR, Western blot, and immunofluorescence staining were performed to observe changes in Bcl-2 family proteins expression. MCAO-damage induced neurobehavioral disorders and chlorogenic acid alleviate these deficits. Bcl-2 and Bcl-xL expressions weredecreased and Bax and Bad expressions were increased in MCAO animals. However, chlorogenic acid treatment attenuated the decreaseof Bcl-2 and Bcl-xL and the increase of Bad and Bax due to MCAO surgery. Moreover, chlorogenic acid treatment attenuatedMCAO-induced upregulation of caspase-3. These findings suggest that chlorogenic acid exerts neuroprotective effects against MCAOdamage by regulating Bcl-2 family proteins including Bcl-2, Bcl-xL, Bax, and Bad.
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