摘要
The expression of BAX in carotid atherosclerosis and its regulation is far from defined. Objectives To investigate BAX expression in stable/fibrous and instable/vulnerable carotid plaque and its clinical significance. Methods 25 cases of carotid plaque specimens obtained from endarterectomy were divided into two groups, stable/fibrous 14 cases, vulnerable/instable 11 cases; aortic artery and its branches from hepatic transplantation donors 6 case as control The expression of proapoptotic BAX was detected by immunohistochemistry （IHC）, in situ hybridization （ISH） and in situ TdT dUTP nick end labeling （TUNEL）. Results 5 cases of BAX （ ＋ ） were detected by ICH and ISH, 4 case of TUNEL （ ＋ ） were detected by TUNEL in stable/fibrous carotid plaque , while 10 cases were BAX （ ＋ ）by IHC（P 〈 0.05 ） , 11 case by ISH and 9 case by TUNEL were detected in instable/vulnerable carotid plaque （P 〈0.01 ）, respectively. The intensity of BAX （ ＋ ） cells by IHC and ISH was 8.63±2.62 and 10.32 ± 3.12 in fibrous plaques,whereas 122 ±21.64 and 152 ± 23.35 in vulnerable plaques, respectively. No expression of BAX was found in controlled group. Conclusion The higher expression of Bax in vulnerable carotid plaque may be one mechanisms in molecular pathogenesis of carotid atherosclerosis which affect plaque stability and be the cause of higher incidence of stroke than fibrous carotid plaques, the regulation of BAX expression in different stage of atherosclerosis may provide targets in gene therapy for carotid atherosclerosis.
The expression of BAX in carotid atherosclcrosis and its regulation is far from defined. Objectives To investigate BAX expression in stable/fibrous and instable/vulnerable carotid plaque and its clinical significance. Methods 25 cases of carotid plaque specimens obtained from endarterectomy were divided into two groups, stable/fibrous 14 cases, vulnerable/instable 11 cases; aortic artery and its branches from hepatic transplantation donors 6 case as control. The expression of proapoptotic BAX was detected by immunohistochemistry (IHC), in situ hybridization(ISH) and in situ TdT dUTP nick end labeling (TUNEL). Results 5 eases of BAX (+) were detected by ICH and ISH, 4 case of TUNEL (+) were detected by TUNEL in stable/fibrous carotid plaque, while 10 cases were BAX (+)by IHC(P<0.05) , 11 case by ISH and 9 case by TUNEL were detected in instable/vulnerable carotid plaque (P<0.01), respectively. The intensity of BAX (+) cells by IHC and ISH was 8.63±2.62 and 10.32±3.12 in fibrous plaques, whereas 122±21.64 and 152±23.35 in vulnerable plaques, respectively. No expression of BAX was found in controlled group. Conclusion The higher expression of Bax in vulnerable carotid plaque may be one mechanisms in molecular pathogenesis of carotid atherosclerosis which affect plaque stability and be the cause of higher incidence of stroke than fibrous carotid plaques, the regulation of BAX expression in different stage of atherosclerosis may provide targets in gene therapy for carotid atherosclerosis.
