AIM OF THE STUDY: Antrodia camphorata (A. camphorata) is well known in Taiwan as a traditional Chinese medicine. The purpose of this study is to evaluate the antioxidant activity of Antrodia camphorata on free radical-induced endothelial cell damage. MATERIALS AND METHODS: In this study, a human umbilical vein endothelial cell (EC) culture system was used to evaluate the effects of the fermented culture broth of A. camphorata (FCBA) and aqueous extracts of mycelia from A. camphorata (AEMA) against the oxidative cell damage induced by the free-radical generator AAPH. RESULTS: The present investigations show that FCBA (25-100 microg/mL) and AEMA (50-200 microg/mL) effectively protect the ECs from damage after exposure to 15 mM AAPH for 16h. However, cell viability was not affected in ECs under controlled conditions after FCBA or AEMA treatment. An increase in EC prostacyclin (PGI(2)) production in response to AAPH exposure was positively and negatively correlated with cell damage and FCBA/AEMA concentration, respectively. Both FCBA and AEMA treatment significantly inhibited AAPH-apoptotic cell death in the ECs, as evidence by reduced DNA fragmentation, cytochrome c release, caspase-3 activation, and dysregulation of Bcl-2 and Bax. Moreover, the AAPH-induced reductions in EC SOD activity and protein levels are prevented by FCBA and AEMA. CONCLUSION: Our findings suggest that A. camphorata possesses antioxidant properties and improves endothelial function, further offering effective protection from atherosclerosis.
AIM OF THE STUDY: Antrodia camphorata (A. camphorata) is well known in Taiwan as a traditional Chinese medicine. The purpose of this study is to evaluate the antioxidant activity of Antrodia camphorata on free radical-induced endothelial cell damage. MATERIALS AND METHODS: In this study, a human umbilical vein endothelial cell (EC) culture system was used to evaluate the effects of the fermented culture broth of A. camphorata (FCBA) and aqueous extracts of mycelia from A. camphorata (AEMA) against the oxidative cell damage induced by the free-radical generator AAPH. RESULTS: The present investigations show that FCBA (25-100 microg/mL) and AEMA (50-200 microg/mL) effectively protect the ECs from damage after exposure to 15 mM AAPH for 16h. However, cell viability was not affected in ECs under controlled conditions after FCBA or AEMA treatment. An increase in EC prostacyclin (PGI(2)) production in response to AAPH exposure was positively and negatively correlated with cell damage and FCBA/AEMA concentration, respectively. Both FCBA and AEMA treatment significantly inhibited AAPH-apoptotic cell death in the ECs, as evidence by reduced DNA fragmentation, cytochrome c release, caspase-3 activation, and dysregulation of Bcl-2 and Bax. Moreover, the AAPH-induced reductions in EC SOD activity and protein levels are prevented by FCBA and AEMA. CONCLUSION: Our findings suggest that A. camphorata possesses antioxidant properties and improves endothelial function, further offering effective protection from atherosclerosis.