PURPOSE:To investigale the influence of orally administered aldose reduetace inhibitor(ARI) and myo-inositol (MI)for contents of gluecose,sorbitol and myo-inositol in experimental diabetic retinal tissue in rat.
METHODS :The STZ-induced diabetic rats were administered ARI or MI by oral. The glucose sorbitol and myo-inositol in retinal tissues were analysed by high performance liquid chromatography after experimental period of 6 montbs. RESULTS:It was found that the contents of glucose and sorhitol were increased and myo inosltol was decreased in diabetic group. In diabetes with ARI group.the content of sorbitol was increased although the glucose was in high level. In diabetes wilb MI group,the sorbitol accumulaled and coment of myo-inositol was close to the normal control group.
CONCLUSIONS:The ARI can effectively obstruct sorbitol accumulation in retina. MI increase myo-inositol level but fail to reduce sorbitol contenl of retina.
（Chin J Ocul Fundus Dis,1997,13: 75-77 ）
ObjectiveTo summarize the changes of gut microbiota after cholecystectomy, the mechanisms of changes, and the relation with colorectal cancer, nonalcoholic fatty liver disease and post-cholecystectomy syndrome after cholecystectomy, in order to provide new ideas for the perioperative management of patients undergoing cholecystectomy. MethodThe studies related to gut microbiota after cholecystectomy at home and abroad were searched and analyzed for review. ResultsThe cholecystectomy disrupted the liver–bile acid–gut flora axis of the patients, and the composition and diversity of the gut microbiota of the patients were altered, and the alteration might lead to the occurrence of colorectal cancer, nonalcoholic fatty liver disease, and post-cholecystectomy syndrome, but the exact mechanism remained unclear. ConclusionsThe balance of intestinal microecology is disrupted after cholecystectomy, and the relation between cholecystectomy and gut microbiota may provide new ideas for the perioperative management of cholecystectomy patients and the prevention and treatment of diseases or symptoms after cholecystectomy, but the effect of cholecystectomy on gut microbiota and the relation with diseases or symptoms still need to be further studied.
To evaluate the cytocompatibil ity of Arg-Gly-Asp-recombinant spider silk protein (pNSR16) / poly vinyl alcohol (PVA) through in vitro cytotoxicity experiment and cell-material co-culture experiment. Methods pNSR16/PVA scaffold and its extraction were prepared by using solvent casting/particulate leaching method, and NIH-3T3 cells were cultivated with the extraction in vitro. The cytotoxicity of scaffold was analyzed using MTT assay 1, 3 and 5 days after culture. Scanning electron microscope and HE staining observation were conducted 2, 4 and 6 days after culturing NIH-3T3 cells on the pNSR16/PVA scaffold. Immunohistochemistry detection was performed 6 days after co-culture. Adhesion, growthand expression of the cells on the scaffold were observed. Results The cytotoxicity of pNSR16/PVA scaffold was in grade 0. Scanning electron microscope observation: the cells covered the surface of the scaffold and were arranged in a directional manner 4 days after co-culture. HE staining: the cells adhered to and grew on the surface of scaffold, and migrated into the scaffold with the increase of culture duration. Immunohistochemistry detection: bFGF was secreted by NIH-3T3 cells, and the cells differentiated normally. Conclusion pNSR16/PVA scaffold has a satisfactory cytocompatibil ity and may be an ideal tissue engineered scaffold materia
ObjectiveTo summarize the epidemiology of nonalcoholic fatty liver disease (NAFLD) and the epidemiological and economic burdens of NAFLD, so as to provide a reference for hospital management decision-making. MethodThe domestic and foreign guidelines relevant to NAFLD and the literatures relevant to epidemiological investigation and disease burden researches were summarized and its research progress was reviewed. ResultsThe global prevalence of NAFLD was increasing over years. The incidence, mortality, and disability adjusted life years of liver cirrhosis and liver cancer caused by NAFLD had increased year by year. The patients relevant to NAFLD of inpatients and outpatients had increased obviously, and the overall medical expenses had also shown a rising trend. The possible reasons were health care awareness, new drug research, population aging, and excessive medical consumption. In addition, children and adolescents with NAFLD had a obviously increased risk of liver or extrahepatic diseases. ConclusionsBy understanding the epidemiological trend of NAFLD, it is a certain understanding of the disease burden of NAFLD and the related factors affecting the increase of its treatment cost. It is believed that it is necessary to further pay attention to and strengthen the genetic characteristics, pathogenesis, drug research and development, and early diagnosis of cirrhosis and liver cancer relevant to NAFLD in the future. At the same time, the NAFLD group of children and adolescents should not be ignored.
1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline (Sal) is a kind of catechol isoquinoline compound, which mainly exists in mammalian brain and performs a variety of biological functions. Through in vivo metabolism, Sal can be transformed into endogenous neurotoxins and can participate the occurrence of Parkinson’s disease (PD). This has attracted widespread concern of researchers. Recently, many research works have shown that Sal may lead to alcohol addiction and regulate hormone release of the neuroendocrine system, which indicated that it is a potential regulator of dopaminergic neurons. In this paper, we discuss the neural functions of Sal on the above aspects, and wish to provide some theoretical supports for further research on its mechanism.
ObjectiveTo summarize the research progress of magnetic resonance imaging (MRI) for diagnosis of nonalcoholic steatohepatitis (NASH).MethodRelevant literatures at home and abroad were collected to make an review, then summarized the research status and progress of MRI for diagnosis of NASH. Their advantages and disadvantages were summarized.ResultsA variety of MRI techniques, including MR elastography, gadolinium-ethoxybenzyldiethylenetriaminepentaacetic acid (Gd-EOB-DTPA) enhanced MRI, diffusion-weighted MR imaging, and quantitative MR imaging of fat and iron, had been widely used in diagnosing NASH and shown to have some value. However, there were currently no effective MRI techniques recommended for diagnosing NASH.ConclusionsMRI plays an important role in noninvasive assessment of NASH. Future studies are needed to investigate more efficient noninvasive biomarkers and models consisting of imaging and non-imaging biomarkers for diagnosing NASH, to reduce unnecessary biopsies.
ObjectiveTo summarize the mechanism of endoplasmic reticulum stress (ERS) in liver diseases. MethodWe sorted out and summarized the studies related to ERS and liver diseases in recent years. ResultsEndoplasmic reticulum plays important roles in protein folding, calcium ion storage, and lipid synthesis in cells. ERS will be induced when the number of misfolded/unfolded proteins in the endoplasmic reticulum increases or the calcium ion homeostasis is unbalanced. The endoplasmic reticulum regulates the unfolded protein response through three transmembrane receptor proteins to initiate corresponding pathways for restoring endoplasmic reticulum homeostasis. Prolonged stress can lead to metabolic disorders. Mild ERS can promote the progression of hepatocellular carcinoma, and continuous ERS will induce cell apoptosis and play an anti-tumor effect; ERS can promote lipid accumulation in non-alcoholic fatty liver disease and aggravate the progression of the disease; in hepatic ischemia reperfusion injury, ERS activation will aggravate liver damage. Meanwhile, ERS activation plays an important pathogenic role in the pathogenesis of drug-induced liver injury. ConclusionERS plays a crucial regulatory role in the occurrence and development of liver-related diseases, providing a theoretical basis and new approach for targeted ERS therapy in liver diseases.
Objective To explore the relationship between different diagnostic criteria (ATPIII2002, IDF2005 and CDS2007 criteria) for metabolic syndrome (MS) and non-alcoholic fatty liver disease (NAFLD). Methods A total of 666 elderly males admitted to West China Hospital for routine physical examination were involved in this study in May, 2010. The diagnostic agreement rates of different criteria were compared, along with the relationship between different diagnostic criteria for MS and NALFD. Results The diagnostic agreement of CDS2007 criteria with either IDF2005 or ATPIII2002 criteria was good. However, the agreement of ATPIII2002 with IDF2005 was compromised. The prevalence of NAFLD in MS group was significantly higher than that of non-MS group (Plt;0.01). On the basis of CDS2007 criteria, there was significant correlation between NAFLD and MS (Plt;0.000). Conclusion There is a close relation between NAFLD and all three diagnostic criteria of MS. NAFLD is one of the most important risk factors of MS. The diagnostic agreement of CDS2007 criteria with the other two is good, and there is significant correlation between NAFLD and criteria CDS2007 of MS. CDS2007 is found to be of high accuracy and applicability in the diagnosis of MS in Chinese population including the elderly.
摘要:目的:探討加蘭他敏對急性酒精中毒大鼠海馬神經元N甲基D天冬氨酸(NMDA)·R2B的影響。 方法:將60只大鼠分為對照組、酒精組及加蘭他敏組,每組各20只。酒精組以50％(v/v) 酒精12 mL/kg灌胃兩次/日,共7d。加蘭他敏組酒精(濃度、劑量同上)灌胃的同時腹腔注射加蘭他敏2mg/kg一次/日,共7d。對照組以等量生理鹽水灌胃。實驗第8天取大鼠海馬區做蘇木精伊紅（HE）染色,觀察海馬區的病理學變化;免疫組織化學采用SABC法,觀察海馬區神經元NR2B的表達。 結果: 病理學觀察結果：對照組海馬區神經細胞排列整齊,胞質淡染,無變性、壞死;酒精組神經細胞層次不清、排列松散、細胞數量減少,部分細胞變性;加蘭他敏組神經細胞層次較清、排列較密,細胞數目較酒精組增; 免疫組織化學結果：酒精組與對照組比較NR2B陽性表達細胞數量明顯減少(Plt;0.01);加蘭他敏組與酒精組比較NR2B陽性表達細胞數量明顯增高(Plt;0.05);加蘭他敏組與對照組比較NR2B表達細胞數量無明顯差異(Pgt;005)。 結論: 急性酒精中毒與海馬區神經細胞的NR2B表達下調有關;加蘭他敏具有保護急性酒精中毒導致的大鼠海馬區神經細胞毒性的作用,其機制可能與加蘭他敏上調NR2B的表達有關。Abstract: Objective: To study the effects of galanthamine on NmethylDaspartic acid receptor 2B (NMDAR2B, NR2B) in the hippocampus (HIP) of acute alcoholism rats. Methods: Total of 60 wistar male rats were randomly divided into control group, ethanol group and glanthamine group, and there were 20 rats in each group. The rats in ethanol group were given by intragastric administration with 50% alcohol (v/v) on the dose of 12 ml/kg twice per day, in control group were given by same dose of saline, and in galanthamine group were treated by intragastric administration with the same concentration and dosage of alcohol as in ethanol group and peritoneal injection with 2 mg/kg of galanthamine once per day for 7 days. In eighth day of experiment, the rats were sacrificed under etherization, and pathological changes of HIP’s zone of rat were observed by HEstaining, and expression of NR2B in neurons of HIP’s zone by immunohistochemical SABC method. Results: The results observed by histopathology showed that in control group, neurons of HIP’s zone lined up in order, cytoplasm had faint staining, and were no degeneration and necrosis; in ethanol group, nerve cells’ layer was unclear, structure was loose, cell number reduced and part of cells degenerated; in galanthamine group, layer of neurons was comparatively clear and arrangement was comparatively dense, and the cell number increased obviously more than ethanol group. The results detected by Immunohistochemistry for NR2B showed that the cell number with expression of NR2B in the HIP’s zone decreased significantly in the ethanol group than in the control group (Plt;0.01), increased in the galanthamine group than in the ethanol group (Plt;0.05), and had no difference between the galanthamin and control group (Pgt;0.05). Conclusion: Acute alcoholism may relate to down regulation of expression of neuron’s NR2B in HIP’s zone;The galanthamin has role of protection for neuron in HIP’s zone induced by toxicity of acute alcoholism, and its mechanism may relate to galanthamin upregulation NR2B expression.
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.
