Gang Li, Jun-Bao Chen, Chao Wang, Zhi Xu, Hao Nie, Xiao-Yan Qin, Xiao-Mei Chen, Quan Gong, Department of Immunology, School of Medicine, Yangtze University, Jingzhou 434023, Hubei Province, China.
World J Gastroenterol. 2013 Nov 14;19(42):7440-6. doi: 10.3748/wjg.v19.i42.7440.
To explore the effects of curcumin (CMN) on hepatic injury induced by acetaminophen (APAP) in vivo.
Male mice were randomly divided into three groups: group I (control) mice received the equivalent volumes of phosphate-buffered saline (PBS) intraperitoneally (ip); Group II [APAP + carboxymethylcellulose (CMC)] mice received 1% CMC (vehicle) 2 h before APAP injection; Group III (APAP + CMN) mice received curcumin (10 or 20 mg/kg, ip) 2 h before before or after APAP challenge. In Groups II and III, APAP was dissolved in pyrogen-free PBS and injected at a single dose of 300 mg/kg. CMN was dissolved in 1% CMC. Mice were sacrificed 16 h after the APAP injection to determine alanine aminotransferase (ALT) levels in serum and malondialdehyde (MDA) accumulation, superoxide dismutase (SOD) activity and hepatocyte apoptosis in liver tissues.
Both pre- and post-treatment with curcumin resulted in a significant decrease in serum ALT compared with APAP treatment group (10 mg/kg: 801.46 ± 661.34 U/L; 20 mg/kg: 99.68 ± 86.48 U/L vs 5406.80 ± 1785.75 U/L, P < 0.001, respectively). The incidence of liver necrosis was significantly lowered in CMN treated animals. MDA contents were significantly reduced in 20 mg/kg CMN pretreatment group, but increased in APAP treated group (10.96 ± 0.87 nmol/mg protein vs 16.03 ± 2.58 nmol/mg protein, P < 0.05). The decrease of SOD activity in APAP treatment group and the increase of SOD in 20 mg/kg CMN pretreatment group were also detected (24.54 ± 4.95 U/mg protein vs 50.21 ± 1.93 U/mg protein, P < 0.05). Furthermore, CMN treatment efficiently protected against APAP-induced apoptosis via increasing Bcl-2/Bax ratio.
CMN has significant therapeutic potential in both APAP-induced hepatotoxicity and other types of liver diseases.
探讨姜黄素（CMN）对体内对乙酰氨基酚（APAP）诱导的肝损伤的影响。
雄性小鼠随机分为三组：I 组（对照组）小鼠腹膜内（ip）给予等体积磷酸盐缓冲盐水（PBS）；II 组[APAP+羧甲基纤维素（CMC）]小鼠在 APAP 注射前 2 小时给予 1%CMC（载体）；III 组（APAP+CMN）小鼠在 APAP 攻击前或后 2 小时给予姜黄素（10 或 20mg/kg，ip）。在 II 组和 III 组中，APAP 溶解在无热原 PBS 中，并以 300mg/kg 的单剂量注射。姜黄素溶解在 1%CMC 中。APAP 注射后 16 小时处死小鼠，以确定血清丙氨酸氨基转移酶（ALT）水平和肝组织中丙二醛（MDA）积累、超氧化物歧化酶（SOD）活性和肝细胞凋亡。
与 APAP 治疗组相比，姜黄素的预处理和后处理均导致血清 ALT 显著降低（10mg/kg：801.46±661.34U/L；20mg/kg：99.68±86.48U/L 与 5406.80±1785.75U/L，P<0.001）。姜黄素处理动物的肝坏死发生率显著降低。20mg/kgCMN 预处理组 MDA 含量显著降低，但 APAP 处理组 MDA 含量升高（10.96±0.87nmol/mg 蛋白与 16.03±2.58nmol/mg 蛋白，P<0.05）。还检测到 APAP 处理组 SOD 活性下降和 20mg/kgCMN 预处理组 SOD 升高（24.54±4.95U/mg 蛋白与 50.21±1.93U/mg 蛋白，P<0.05）。此外，CMN 处理通过增加 Bcl-2/Bax 比值有效保护 APAP 诱导的凋亡。
CMN 对 APAP 诱导的肝毒性和其他类型的肝病具有显著的治疗潜力。
