ne 10010110210310 100101102103104 100101102103104 dioc6(3) f 它山山 10°101102103104 100101102103104 10010110210310 dioc6 dioc6( dioc6(3 Effect of glucose deprivation on the mitochondrial transmembrane potential(Aym) of PC12 cells. (a)control cells (b)cells treated with 100HM carbonyl cyanide chlorophenylhydrazone(cccp) to fully depolarize mitochondria(c)glucose treatment for 3 hours (d)glucose treatment for 6 hours(e) glucose treatment for 24 hours(f glucose treatment for 48 hours
Effect of glucose deprivation on the mitochondrial transmembrane potential(Δψm) of PC12 cells.(a) control cells (b) cells treated with 100μM carbonyl cyanide chlorophenylhydrazone(CCCP) to fully depolarize mitochondria (c) glucose treatment for 3 hours (d) glucose treatment for 6 hours (e) glucose treatment for 24 hours (f) glucose treatment for 48 hours
与细胞死亡有关的线粒体机制 活性氧在启动和调节细胞凋亡过程中扮演着 重要角色 MPTP是细胞凋亡的环节之一 细胞色素c渗漏到胞质可以导致细胞凋亡 Bcl-2家族对细胞凋亡过程实施着调控 ※p53蛋白易位也是控制细胞凋亡的重要途径
与细胞死亡有关的线粒体机制 活性氧在启动和调节细胞凋亡过程中扮演着 重要角色 MPTP是细胞凋亡的环节之一 细胞色素c渗漏到胞质可以导致细胞凋亡 Bcl-2家族对细胞凋亡过程实施着调控 p53蛋白易位也是控制细胞凋亡的重要途径
FasI Fig 2. Schematic presentation of the Fas/caspase, Bel-2/mitochondrial, and nuclear p53 death-regulating pathways Fas Cellular membrane Bele2 BAD FADD BID Caspase-8 8 Caspase- zymogen Mitochondrium Cvt-C APAF-I C zymogen Substrate cleavage OSIS uncle DNA damage year
Cell death signal Cell death siona 世3- only proteins Ceramide, Ca2+ and other PTP openers. Bcl-2 but neither Bax nor Bak Bax/ Bak Bcl-x Bcl-2 BClXL Open PTP Competence to die by apoptosIs? Yes No Moderate*△mt Sewvereya'm and ATP ss and ATP loss Caspase activatIo Caspase-independar cell death/ necosi Apoptosi
I Proposed scheme for the mAchanism of pore apening Stalag d 骑持 心 AAFc :君 Creat Jyh CoMt Meas,nMet 和2 u : Mt-:H 6可b tna: itwwtvmne Ji cas心2 护A