AIM: To investigate the anti-fibrosis effect of IκB kinase-beta inhibitor (IKK2 inhibitor IMD0354) in liver fibrosis. METHODS: Twenty male C57BL6 mice were divided into four groups. Five high-fat fed mice were inject...AIM: To investigate the anti-fibrosis effect of IκB kinase-beta inhibitor (IKK2 inhibitor IMD0354) in liver fibrosis. METHODS: Twenty male C57BL6 mice were divided into four groups. Five high-fat fed mice were injected with lipopolysaccharide (LPS, 10 mg/kg) intraperitoneally and five high-fat fed mice were without LPS injection to build models of liver injury, and the intervention group (five mice) was injected intraperitoneally with IKK2 inhibitor (IMD 30 mg/kg for 14 d), while the remaining five mice received a normal diet as controls. Hepatic function, pathological evaluation and liver interleukin-6 (IL-6) expression were examined. Western blotting and real-time polymerase chain reaction were used to detect the expressions of nuclear factor-κB (NF-κB), alpha-smooth muscle actin (α-SMA), tumor growth factor-beta1 (TGF-β1), tumor necrosis factor-alpha (TNF-α), typeⅠand type Ⅲ collagen proteins and mRNA. RESULTS: A mouse model of liver injury was successfully established, and IMD decreased nuclear transloca-tion of NF-κB p65 in liver cells. In the IMD-treated group, the levels of alanine aminotransferase (103 ± 9.77 μ/L vs 62.4 ± 7.90 μ/L, P < 0.05) and aminotransferase (295.8 ± 38.56 μ/L vs 212 ± 25.10 μ/L, P < 0.05) were significantly decreased when compared with the model groups. The histological changes were significantly ameliorated. After treatment, the expressions of IL-6 (681 ± 45.96 vs 77 ± 7.79, P < 0.05), TGF-β1 (Western blotting 5.65% ± 0.017% vs 2.73% ± 0.005%, P < 0.05), TNF-α (11.58% ± 0.0063% vs 8.86% ± 0.0050%, P < 0.05), typeⅠcollagen (4.49% ± 0.014% vs 1.90% ± 0.0006%, P < 0.05) and type Ⅲ collagen (3.46% ± 0.008% vs 2.29% ± 0.0035%, P < 0.05) as well as α-SMA (6.19 ± 0.0036 μ/L vs 2.16 ± 0.0023 μ/L, P < 0.05) protein and mRNA were downregulated in the IMD group compared to the fibrosis control groups (P < 0.05). CONCLUSION: IKK2 inhibitor IMD markedly improved non-alcoholic fatty liver disease in mice by lowering NF-κB activation, which could become a 展开更多
目的检测C57BL/6小鼠无创性肺功能指标,为小鼠实验性研究肺功能的监测提供依据。方法采用整体体积描记法(whole body plethysmography,WBP)检测460只C57BL/6小鼠肺功能的各项指标,对检测结果进行统计分析,百分位数法确定参考值范围。结...目的检测C57BL/6小鼠无创性肺功能指标,为小鼠实验性研究肺功能的监测提供依据。方法采用整体体积描记法(whole body plethysmography,WBP)检测460只C57BL/6小鼠肺功能的各项指标,对检测结果进行统计分析,百分位数法确定参考值范围。结果小鼠吸气时间(Ti)64.7(55.30～82.60)ms,呼气时间(Te)83.4(71.70～109.20)ms,呼气峰值时间比率(Rpef)0.21(0.16～0.28),吸气末端暂停(EIP)2.19(1.96～3.76)ms,呼气末暂停(EEP)1.67(0.12～9.15)ms,潮气量(TVb)0.44(0.25～0.58)mL,气道狭窄指数(Penh)1.29(0.91～2.00),呼吸暂停(PAU)1.18(1.00～1.64),呼气中期流速(EF50)0.64(0.30～0.98)mL/s,松弛时间(Tr)39.0(32.40～51.50)ms,最大吸气流速(PIF)9.74(5.33～12.83)mL/s,最大呼气流速(PEF)9.86(5.12～13.47)mL/s,呼吸频率(f)412(331～474)BPM,每分钟通气量(MVb)174.4(86.69～235.04)mL。结论 C57BL/6小鼠无创肺功能指标参考值范围的测定,可为呼吸系统疾病的基础研究提供实验性参考依据。展开更多
基金Supported by Shanghai Municipal Health Bureau Youth Grant, No. 2008Y032
文摘AIM: To investigate the anti-fibrosis effect of IκB kinase-beta inhibitor (IKK2 inhibitor IMD0354) in liver fibrosis. METHODS: Twenty male C57BL6 mice were divided into four groups. Five high-fat fed mice were injected with lipopolysaccharide (LPS, 10 mg/kg) intraperitoneally and five high-fat fed mice were without LPS injection to build models of liver injury, and the intervention group (five mice) was injected intraperitoneally with IKK2 inhibitor (IMD 30 mg/kg for 14 d), while the remaining five mice received a normal diet as controls. Hepatic function, pathological evaluation and liver interleukin-6 (IL-6) expression were examined. Western blotting and real-time polymerase chain reaction were used to detect the expressions of nuclear factor-κB (NF-κB), alpha-smooth muscle actin (α-SMA), tumor growth factor-beta1 (TGF-β1), tumor necrosis factor-alpha (TNF-α), typeⅠand type Ⅲ collagen proteins and mRNA. RESULTS: A mouse model of liver injury was successfully established, and IMD decreased nuclear transloca-tion of NF-κB p65 in liver cells. In the IMD-treated group, the levels of alanine aminotransferase (103 ± 9.77 μ/L vs 62.4 ± 7.90 μ/L, P < 0.05) and aminotransferase (295.8 ± 38.56 μ/L vs 212 ± 25.10 μ/L, P < 0.05) were significantly decreased when compared with the model groups. The histological changes were significantly ameliorated. After treatment, the expressions of IL-6 (681 ± 45.96 vs 77 ± 7.79, P < 0.05), TGF-β1 (Western blotting 5.65% ± 0.017% vs 2.73% ± 0.005%, P < 0.05), TNF-α (11.58% ± 0.0063% vs 8.86% ± 0.0050%, P < 0.05), typeⅠcollagen (4.49% ± 0.014% vs 1.90% ± 0.0006%, P < 0.05) and type Ⅲ collagen (3.46% ± 0.008% vs 2.29% ± 0.0035%, P < 0.05) as well as α-SMA (6.19 ± 0.0036 μ/L vs 2.16 ± 0.0023 μ/L, P < 0.05) protein and mRNA were downregulated in the IMD group compared to the fibrosis control groups (P < 0.05). CONCLUSION: IKK2 inhibitor IMD markedly improved non-alcoholic fatty liver disease in mice by lowering NF-κB activation, which could become a
文摘目的检测C57BL/6小鼠无创性肺功能指标,为小鼠实验性研究肺功能的监测提供依据。方法采用整体体积描记法(whole body plethysmography,WBP)检测460只C57BL/6小鼠肺功能的各项指标,对检测结果进行统计分析,百分位数法确定参考值范围。结果小鼠吸气时间(Ti)64.7(55.30～82.60)ms,呼气时间(Te)83.4(71.70～109.20)ms,呼气峰值时间比率(Rpef)0.21(0.16～0.28),吸气末端暂停(EIP)2.19(1.96～3.76)ms,呼气末暂停(EEP)1.67(0.12～9.15)ms,潮气量(TVb)0.44(0.25～0.58)mL,气道狭窄指数(Penh)1.29(0.91～2.00),呼吸暂停(PAU)1.18(1.00～1.64),呼气中期流速(EF50)0.64(0.30～0.98)mL/s,松弛时间(Tr)39.0(32.40～51.50)ms,最大吸气流速(PIF)9.74(5.33～12.83)mL/s,最大呼气流速(PEF)9.86(5.12～13.47)mL/s,呼吸频率(f)412(331～474)BPM,每分钟通气量(MVb)174.4(86.69～235.04)mL。结论 C57BL/6小鼠无创肺功能指标参考值范围的测定,可为呼吸系统疾病的基础研究提供实验性参考依据。
