目的綜述酒精性股骨頭缺血性壞死(osteonecrosis of the femoral head,ONFH)的研究進展。 方法廣泛查閱國內外近年與酒精性ONFH相關的文獻,并進行總結分析。 結果酒精性ONFH患者約占ONFH患者的1/3。研究表明,酒精攝入量與ONFH發病具有明顯量效關系,酒精性ONFH發生與患者脂代謝、糖皮質激素分泌有關,與脂質和酒精代謝性基因存在相關性。 結論酒精與脂代謝、激素的關系與作用機制仍是研究主要方向,基因水平研究尚不能闡釋發病機制,仍需深入研究。
【摘要】 目的 研究2型糖尿病(type 2 diabetes mellitus,T2DM)合并非酒精性脂肪性肝病(non-alcoholic fatty liver disease, NAFLD)患者血漿脂肪細胞特異性脂肪酸結合蛋白(adipocyte-specific fatty acid-binding protein,A-FABP)的水平及其相關因素。 方法 2009年10月—2010年10月選取T2DM合并NAFLD組(A組)60例,未合并NAFLD組56例(B組)為研究對象。測定體質量指數(body mass index,BMI),檢測血脂、糖化血紅蛋白(hemoglobin A1c,HbA1c)等生化指標。放射免疫法測定空腹胰島素(fasting insulin,FINS),空腹C肽水平(fasting C-peptide,FCP),計算胰島素抵抗指數(homeostasis model of assessment-insulin resistance,HOMA-IR)、胰島素敏感指數(insulin sensitivity index,ISI),測定A-FABP、C反應蛋白(C-reaction protein,CRP)及腫瘤壞死因子-α(tumor necrosis factor-α,TNF-α)。 結果 與B組患者相比,A組患者其血漿A-FABP水平、BMI、腰圍、腰臀比、丙氨酸氨基轉移酶、門冬氨酸氨基轉移酶、CRP、TNF-α、FCP、FINS、總膽固醇、甘油三酯、Ln(HOMA-IR)升高,Ln(ISI)降低,差異有統計學意義(Plt;0.05);兩組HbA1c差異無統計學意義(Pgt;0.05)。A-FABP水平變化與TNF-α、HOMA-IR、CRP呈正相關,與ISI呈負相關。 結論 T2DM伴NAFLD中,A-FABP升高與胰島素抵抗是并存的,且存在明顯相關關系,二者在疾病的發生發展中均可能具有重要的作用。【Abstract】 Objective To analyze the serum level of adipocyte-specific fatty acid-binding protein (A-FABP) in patients with type 2 diabetes mellitus (T2DM) complicated with non-alcoholic fatty liver disease (NAFLD), and its related factors. Methods From October 2009 to October 2010, 112 patients with T2DM were categorized into two groups: the group with NAFLD (group A) with 60 patients, and the group without NAFLD (group B) with 56 patients. Body mass index (BMI), alanine aminotransferase (ALT), aspartate aminotransferase (AST), total cholesterol (TC), triglyceride (TG), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), and hemoglobin A1c (HbA1c) were detected. Radioimmunoassay was carried out to measure fasting insulin (FINS) and fasting C-peptide (FCP), and homeostasis model of assessment-insulin resistance (HOMA-IR) and insulin sensitivity index (ISI) were calculated. At the same time, A-FABP, C-reaction protein (CRP) and tumor necrosis factor-α (TNF-α) were also detected. Results Compared with patients in group B, plasma levels of A-FABP, BMI, waistline, waist to hip ratio, ALT, AST, TG, TC, HDL-C, LDL-C, CRP, FCP, FINS, and HOMA-IR for patients in group A were all higher, while ISI was lower; and the differences in the above-mentioned parameters were statistically significant (Plt;0.05). The levels of HbA1c in the two groups were not significantly different (Pgt;0.05). The change of A-FABP level was positively correlated with TNF-α, HOMA-IR and CRP, while it wasnegatively correlated with ISI. Conclusions In patients with T2DM with NAFLD, there is an obvious correlation between the coexisting A-FABP rise and insulin resistance. Both of them played critical roles in the onset and developing of the disease.
【摘要】 目的 觀察長期大量酒精攝入對大鼠心肌結構及心肌組織中丙二醛(MDA)、超氧化物歧化酶(SOD)和金屬硫蛋白(MT)含量的影響,探討氧化應激在酒精性心肌病大鼠中的作用。 方法 雄性健康SD大鼠45只,隨機分為2組,即對照組20只和模型組25只。模型組酒精濃度從5%、10%、20%和30%依次各自由飲1周,然后遞增至36%后以該濃度維持飼喂。對照組每日飲用與模型組酒精同等熱量的葡萄糖水。6個月后,觀察大鼠心肌組織的形態學改變及超微結構的變化,測定心肌組織中MDA、SOD及MT的含量。結果 模型組大鼠心肌細胞排列紊亂、間質充血、炎細胞浸潤、線粒體腫脹、空泡形成、肌絲溶解、核膜不規則和核仁裂解。心肌組織中MDA含量明顯升高(Plt;0.01),SOD活力含量明顯降低(Plt;0.01),MT含量明顯降低(Plt;0.01)。 結論 長期攝入大量酒精可使氧自由基代謝失衡,導致心肌損傷。氧化應激在酒精性心肌病發病機制中發揮著重要的作用。【Abstract】 Objective To observe the effect of longterm and large quantities of alcohol intake on myocardial structure of rats and the content of malondialdehyde (MDA), superoxide dismutase (SOD) and metallothionein (MT) in myocardium tissue. To study the effect of oxidative stress on the rats with alcoholic cardiomyopathy. Methods Fortyfive male and healthy SD rats were randomly divided into the control group (20 rats) and model group (25 rats).The alcoholic concentrate in model group was increased from 5%,10%,20% to 30% every week, and maintain free drinking mass concentration of 36% alcohol. The control group drink the same calories of glucose water. Six months later, the myocardial tissues were observed both in light microscope and electron microscope .The level of MDA、SOD and MT were tested in myocardium tissue. Results In the model rats, the cells of myocardial disarray, interstitial congestion, inflammatory cell infiltration, mitochondrial swelling, vacuole formation, melt filaments, irregular nuclear membrane and nucleolus cracking. The content of MDA incresed(Plt;0.01)and the activities of SOD decreased(Plt;001),levels of MT decreased (Plt;0.01) in the cardiac muscular tissues in the model group compared with the control group. Conclusion Longterm intake of large amounts of alcohol can break the balance of oxygen free radicals, which leading to the damage of myocardial. Oxidative stress plays an important role in the etiopathogenesis of alcoholic cardiomyopathy.
摘要:目的: 研究蛻皮甾酮對非酒精性脂肪性肝病大鼠模型腫瘤壞死因子α(TNFα)與核因子κB(NFκB)表達的影響,并探索其可能的作用機制。 方法 :健康成年SD大鼠36只,隨機分為正常對照組12只與實驗組24只;正常對照組喂以普通基礎飼料,實驗組應用高脂飼料喂養。實驗12周末時將造模成功的實驗組大鼠隨機分為模型組與蛻皮甾酮治療組2個亞組,每組12只;正常對照組喂以普通基礎飼料至16周,模型組繼續應用改良高脂飼料喂養至16周,蛻皮甾酮治療組大鼠在高脂飲食同時加用蛻皮甾酮灌胃。實驗16周末時處死3組所有大鼠;檢測肝臟指數,血清與肝組織生化指標及肝組織病理改變;ELISA法檢測肝臟TNFα水平;免疫組化檢測各組大鼠肝組織中核因子κB蛋白表達情況。 結果 :蛻皮甾酮治療組血清膽固醇(TC)、丙氨酸氨基轉移酶(ALT)和天門冬氨酸氨基轉移酶(AST)明顯低于模型組(212±058比263±024,Plt;005;5336±1848比8460±3627,P<005;14020±3595比24359±3638,P<001);蛻皮甾酮治療組與模型組相比肝組織丙二醛(MDA)水平降低明顯(18454±1645比23928±2376,P<001),超氧化物歧化酶(SOD)活力增加顯著(942±052比518±043,P<001),肝臟指數顯著降低(435±037比504±046,P<001),肝組織脂肪變性程度和炎癥活動度明顯減輕(546±037比630±049,P<001)。蛻皮甾酮治療組與模型組相比TNFα與核因子κB水平明顯減輕(4304±748比6156±727,2465±539比4504±746,P值均<001)。 結論 :蛻皮甾酮具有改善高脂飲食誘發的非酒精性脂肪性肝病大鼠肝臟酶學功能,通過增加肝組織SOD的含量和減少MDA的含量來減輕肝組織氧化應激水平,減輕肝組織TNFα和核因子κB來減輕肝臟炎癥,發揮防治非酒精性脂肪性肝病的作用。Abstract: Objective: To investigate the effect and possible mechanism of ecdysterone on the expression of tumor necrosis factoralpha (TNFα) and nuclear factor κ B (NFκB) in rats with nonalcoholic fatty liver disease of rats. Methods : A total of 36 male Sprague Dawley rats were randomly divided into two groups, who were fed with highfat diet (experimental group, n=24) and normal basic food (normal control, n=12) respectively. At the end of the 12th week, the experimental group was randomly divided into two subgroups: model group and ecdysterone group, each group contained 12 rats. From the 13th week, the rats in the normal control group and model group were lavaged with normal sodium, and the rats in the ecdysterone group were lavaged with ecdysterone at 10 mg·kg-1·d-1. At the end of the 16th week, all rats were weighed, narcotized, sacrificed, and the liver index, biochemical indicators in serum and liver tissues and the hepatic pathological changes were observed. The expression of TNFα was detected by ELISA and the expression of NFκB was measured by immunohistochemical staining. Results : At the end 16th week in ecdysterone group, the serum levels of cholesterol (TC), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were reduced markedly (212±058 vs 263±024 and 5336±1848 vs 8460±3627, both P<005; 14020±3595 vs 24359±3638, P<001); the tissue content of malondialdehyde (MDA) was decreased evidently (18454±1645 vs 23928±2376, P<001), while the activity of superoxide dismutase (SOD) was enhanced notably (942±052 vs 518±043, P<001); the liver index was decreased significantly in comparison with that inmodel group (435±037 vs 504±046, P<001); the degree of fatty degeneration and inflammation were relieved dramatically (546±037 vs 630±049, P<001). The expression of TNFα and the levels of NFκB were significantly lower (4304±748 vs 6156±727 and 2465±539 vs 4504±746, both P<001) in ecdysterone group compared with model group. Conclusion : The effects of ecdysterone in preventing NAFLD in rats could be related to the increase of SOD content in hepatic tissue and the decrease of MDA content, tumor necrosis factorα and NFκB.