AIM: To assess vitamin D (Vit D) abnormalities in hepatitis C infected patients and their relationship with interleukin (IL)-17, IL-23 and N-terminal propeptide of type Ⅲ pro-collagen (PⅢNP) as immune response media...AIM: To assess vitamin D (Vit D) abnormalities in hepatitis C infected patients and their relationship with interleukin (IL)-17, IL-23 and N-terminal propeptide of type Ⅲ pro-collagen (PⅢNP) as immune response mediators. METHODS: The study was conducted on 50 Egyptian patients (36 male, 14 female) with hepatitis C virus (HCV) infection, who visited the Hepatology Outpatient Clinic in the Endemic Disease Hospital at Cairo University. Patients were compared with 25 ageand sexmatched healthy individuals. Inclusion criteria were based on a history of liver disease with HCV genotype 4 (HCV-4) infection (as new patients or under followup). Based on ultrasonography, patients were classified into four subgroups; 14 with bright hepatomegaly; 11 with perihepatic fibrosis; 11 with hepatic cirrhosis; and 14 with cirrhosis and hepatocellular carcinoma (HCC).Total Vit D (i.e., 25-OH-Vit D) and active Vit D [i.e., 1,25-(OH) 2 -Vit D] assays were carried out using commercial kits. IL-17, IL-23 and PⅢNP levels were assayed using enzyme linked immunosorbent assay kits, while HCV virus was measured by quantitative and qualitative polymerase chain reaction. RESULTS: Levels of Vit D and its active form were significantly lower in advanced liver disease (hepatic cirrhosis and/or carcinoma) patients, compared to those with bright hepatomegaly and perihepatic fibrosis. IL-17, IL-23 and PⅢNP levels were markedly increased in HCV patients and correlated with the progression of hepatic damage. The decrease in Vit D and active Vit D was concomitant with an increase in viral load, as well as levels of IL-17, IL-23 and PⅢNP among all subgroups of HCV-infected patients, compared to normal healthy controls. A significant negative correlation was evident between active Vit D and each of IL-17, IL-23 and PⅢNP (r = -0.679, -0.801 and -0.920 at P < 0.001, respectively). HCV-infected men and women showed no differences with respect to Vit D levels. The viral load was negatively correlated with Vit D and active Vit D (r = -0.084 and -0.846 at P < 0.001, respectively), and positively correlated with IL-17, IL-23 and PⅢNP (r = 0.951, 0.922 and 0.94 at P < 0.001, respectively). Whether the deficiency in Vit D was related to HCVinduced chronic liver disease or was a predisposing factor for a higher viral load remains to be elucidated. CONCLUSION: The negative correlations between Vit D and IL-17, IL-23 and PⅢNP highlight their involvement in the immune response in patients with HCV-4related liver diseases in Egypt.展开更多
目的:通过观察全反式维甲酸对慢性酒精性肝损伤大鼠肝脏TGF-β1、CTGF和Collal表达的影响,探讨该药物对酒精性肝纤维化形成的作用．方法:大鼠24只随机分为3组:酒精组(J组),给予酒精-玉米油混悬液灌胃;治疗组(A组),给予上述混悬液灌胃8 w...目的:通过观察全反式维甲酸对慢性酒精性肝损伤大鼠肝脏TGF-β1、CTGF和Collal表达的影响,探讨该药物对酒精性肝纤维化形成的作用．方法:大鼠24只随机分为3组:酒精组(J组),给予酒精-玉米油混悬液灌胃;治疗组(A组),给予上述混悬液灌胃8 wk后加用0,15 mg／(kg·d) 的全反式维甲酸灌胃;对照组(N组),给予等量的生理盐水和玉米油灌胃．16 wk后处死大鼠．光、电镜下观察肝组织病理改变,高压液相色谱法(HPLC)测肝组织中维甲酸的含量,免疫组化法检测肝组织中转化生长因子β1(TGF-β1)和结缔组织生长因子(CTGF)的蛋白水平,逆转录聚合酶链反应(RT-PCR)检测肝组织中TGF-β1、CTGF和Ⅰ型胶原前胶原α1(Collal)的mRNA水平．结果:光镜下酒精组及治疗组均呈不同程度的酒精性肝炎改变,电镜下酒精组肝细胞线粒体肿胀,内质网扩张,脱颗粒,而治疗组改变轻于酒精组．肝组织中维甲酸含量:酒精组低于正常组,治疗组接近对照组水平．Collal 的mRNA表达在酒精组中较对照组明显增高 (0．18±0．03 vs 0．10±0．02,P<0．01),治疗组较酒精组表达下降(0．14±0．03 vs 0．18±0．03,P <0．05)．TGF-β1的mRNA及蛋白表达在酒精组中增高(0．53±0．17 vs 0．34±0．05,105．93 ±10．12 vs 149．27±10．17,P<0．01),治疗组相对于酒精组有所下降(0．41±0．06 vs 0．53± 0．17,130．80±6.23 vs 105．93±10．12,P<0．05)． CTGF的mRNA及蛋白表达在酒精组中增高 (0．41±0．13 vs 0．17±0．05,130．84±5．72 vs 158.37±6．64,P<0．05),治疗组对于酒精组有所下降(0.30±0．04 vs 0．41±0．13,149．23± 6．65 vs 130．84±5．72．P<0．05)．结论:小剂量全反式维甲酸通过降低慢性酒精性肝损伤大鼠肝脏致纤维化因子TGF-β1, CTGF和Collal的表达抑制早期酒精性肝纤维化的形成．展开更多
文摘AIM: To assess vitamin D (Vit D) abnormalities in hepatitis C infected patients and their relationship with interleukin (IL)-17, IL-23 and N-terminal propeptide of type Ⅲ pro-collagen (PⅢNP) as immune response mediators. METHODS: The study was conducted on 50 Egyptian patients (36 male, 14 female) with hepatitis C virus (HCV) infection, who visited the Hepatology Outpatient Clinic in the Endemic Disease Hospital at Cairo University. Patients were compared with 25 ageand sexmatched healthy individuals. Inclusion criteria were based on a history of liver disease with HCV genotype 4 (HCV-4) infection (as new patients or under followup). Based on ultrasonography, patients were classified into four subgroups; 14 with bright hepatomegaly; 11 with perihepatic fibrosis; 11 with hepatic cirrhosis; and 14 with cirrhosis and hepatocellular carcinoma (HCC).Total Vit D (i.e., 25-OH-Vit D) and active Vit D [i.e., 1,25-(OH) 2 -Vit D] assays were carried out using commercial kits. IL-17, IL-23 and PⅢNP levels were assayed using enzyme linked immunosorbent assay kits, while HCV virus was measured by quantitative and qualitative polymerase chain reaction. RESULTS: Levels of Vit D and its active form were significantly lower in advanced liver disease (hepatic cirrhosis and/or carcinoma) patients, compared to those with bright hepatomegaly and perihepatic fibrosis. IL-17, IL-23 and PⅢNP levels were markedly increased in HCV patients and correlated with the progression of hepatic damage. The decrease in Vit D and active Vit D was concomitant with an increase in viral load, as well as levels of IL-17, IL-23 and PⅢNP among all subgroups of HCV-infected patients, compared to normal healthy controls. A significant negative correlation was evident between active Vit D and each of IL-17, IL-23 and PⅢNP (r = -0.679, -0.801 and -0.920 at P < 0.001, respectively). HCV-infected men and women showed no differences with respect to Vit D levels. The viral load was negatively correlated with Vit D and active Vit D (r = -0.084 and -0.846 at P < 0.001, respectively), and positively correlated with IL-17, IL-23 and PⅢNP (r = 0.951, 0.922 and 0.94 at P < 0.001, respectively). Whether the deficiency in Vit D was related to HCVinduced chronic liver disease or was a predisposing factor for a higher viral load remains to be elucidated. CONCLUSION: The negative correlations between Vit D and IL-17, IL-23 and PⅢNP highlight their involvement in the immune response in patients with HCV-4related liver diseases in Egypt.
文摘目的:通过观察全反式维甲酸对慢性酒精性肝损伤大鼠肝脏TGF-β1、CTGF和Collal表达的影响,探讨该药物对酒精性肝纤维化形成的作用．方法:大鼠24只随机分为3组:酒精组(J组),给予酒精-玉米油混悬液灌胃;治疗组(A组),给予上述混悬液灌胃8 wk后加用0,15 mg／(kg·d) 的全反式维甲酸灌胃;对照组(N组),给予等量的生理盐水和玉米油灌胃．16 wk后处死大鼠．光、电镜下观察肝组织病理改变,高压液相色谱法(HPLC)测肝组织中维甲酸的含量,免疫组化法检测肝组织中转化生长因子β1(TGF-β1)和结缔组织生长因子(CTGF)的蛋白水平,逆转录聚合酶链反应(RT-PCR)检测肝组织中TGF-β1、CTGF和Ⅰ型胶原前胶原α1(Collal)的mRNA水平．结果:光镜下酒精组及治疗组均呈不同程度的酒精性肝炎改变,电镜下酒精组肝细胞线粒体肿胀,内质网扩张,脱颗粒,而治疗组改变轻于酒精组．肝组织中维甲酸含量:酒精组低于正常组,治疗组接近对照组水平．Collal 的mRNA表达在酒精组中较对照组明显增高 (0．18±0．03 vs 0．10±0．02,P<0．01),治疗组较酒精组表达下降(0．14±0．03 vs 0．18±0．03,P <0．05)．TGF-β1的mRNA及蛋白表达在酒精组中增高(0．53±0．17 vs 0．34±0．05,105．93 ±10．12 vs 149．27±10．17,P<0．01),治疗组相对于酒精组有所下降(0．41±0．06 vs 0．53± 0．17,130．80±6.23 vs 105．93±10．12,P<0．05)． CTGF的mRNA及蛋白表达在酒精组中增高 (0．41±0．13 vs 0．17±0．05,130．84±5．72 vs 158.37±6．64,P<0．05),治疗组对于酒精组有所下降(0.30±0．04 vs 0．41±0．13,149．23± 6．65 vs 130．84±5．72．P<0．05)．结论:小剂量全反式维甲酸通过降低慢性酒精性肝损伤大鼠肝脏致纤维化因子TGF-β1, CTGF和Collal的表达抑制早期酒精性肝纤维化的形成．
