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.
Objective To investigate the influence of chronic alcohol ingestion on the severity of acute lung injury (ALI) induced by oleic acid and lipopolysaccharide (LPS).Methods Thirty-two SD rats were randomly administrated with alcohol or water for 6 weeks，then instilled with oleic acid and LPS to induce ALI or with normal saline as control.Thus the rats were randomly divided into two injury groups [ethanol group and water group] and two control groups [ethanol group and water group] (n=8 in each group). PaO2,Wet to dry lung weight ratio (W/D)，levels of γ-glutamylcysteinylglycine (GSH) and malonaldehyde (MDA) in the lung tissue were measured.Results Compared to corresponding control groups，the PaO2 and GSH significantly decreased，and the lung W/D and MDA level were significantly increased in the injury groups (all Plt;0.05).In the injury groups，the changes of above parameters were more significant in the alcohol group than thoe in the water group (all Plt;0.05)，except the lung W/D with no significant difference.Conclusion Chronic ethanol ingestion was relevalent to oxidation/ antioxidation imbalance and more severe lung injury in rats with severe septic after trauma,which suggests that chronic alcohol abuse could increase the severity of acute lung injury.
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:探討納絡酮對急性酒精中毒的臨床療效及經驗。方法: 將58例酒精中毒患者隨機分為2組:常規治療組29例,給予利尿劑、胃腸黏膜保護劑及靜脈補液對癥治療;納絡酮治療組29例,除了應用常規治療方法外,加用納絡酮。結果:納絡酮治療組患者癥狀改善,清醒時間明顯提前于對照組(Plt;0.01)。結論: 納絡酮治療急性酒精中毒療效肯定、使用簡單安全,值得臨床推廣使用。Abstract: Objective: To evaluate the clinical effect of naoxone on acute alcoholism. Methods: Fiftyeight cases of acute alcoholism were randomly divided into two groups: remedial group (29 cases) and the comparison group (29 cases). Both groups were given diuretic, protection of mucous membrane of stomach and fluid infusion. The remedial group was treated with naloxone. Results: Symptoms of the remedial group were obviously improved. Consciousness was regained much earlier than that of the comparison group (Plt;0.01). Conclusion: Naloxone can be used effectively and safely in treating acute alcoholism.
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.
The mechanisms of general anesthesia, which was introduced about 170 years ago, remain poorly understood. Even less well understood are the effects of general anesthesia on the human body. Recently we identified 18 G-protein coupled receptor (GPCR) genes of Daphnia pulex, an invertebrate model organism. Phylogenetic analysis identified these genes to be the homologs of the human γ-aminobutyric acid, type B (GABAB) receptor, metabotropic glutamate receptors (mGluR), adrenergic receptor, serotonin (5-HT) receptor, dopamine receptor and muscarinic acetylcholine receptor (mAChR). Using reverse transcription and quantitative PCR techniques, we systematically measured the effects of propofol, etomidate and ethanol on these 18 GPCR mRNA expressions in Daphnia pulex.
【Abstract】 Objective To measure the changes of bone mineral density and bone micro-architecture of thefemoral head that harvested from the three-foot bearing ethanol destroyed canine model for osteonecrosis of femoral head, and discuss the influences of local injection of ethanol and biomechanical loading to the structural properties of the femoral head. Methods Twenty-four Beagles were divided randomly into four-foot bearing canines and three-foot bearing canines. One fore-l imb was fixed randomly in three-foot bearing canines. Osteonecrosis was induced in all experimental animals by local injection of 5 mL pure ethanol into one side of the femoral head. The hind l imbs injected with NS were acted as control group, that of three-foot canines injected with ethanol were acted as three-foot canine group, and that of four-foot canines injected with ethanol were acted as four-foot canine group. The contralateral femoral head was injected into equal amount of NS. Animals were sacrificed at the time intervals of 1, 3, 6, and 12 weeks after the injection of ethanol. Quantitative microcomputedtomography was used to characterize changes in bone micro-architecture and bone mineral density of femoralhead. Results The clear three-dimensional model of trabecular bone of necrotic femoral head were obtained. There were no significant differences among 3 groups according to the time l ine by 1 week after ethanol injection(P gt; 0.05). At 3 weeks after injection of ethanol, in three-foot canine group and four-foot canine group, the volume of BMC, BMD, BVF, and BS/BV increased gradually as the distance to the drill ing canal increased. There were significant differences between 3 regions (P lt; 0.05). At 6 weeks, in three-foot canine group and four-foot canine group, the volume of BMC, BMD,BVF, and Tb.N of region I and II decreased significantly compared with region III (P lt; 0.05). At 12 weeks, there are no differences among 3 groups (P gt; 0.05). There were significant decreases in BMD values, BVF, BS/BV, Tb.N, Tb.Sp and Tb.Th after the injection of pure ethanol. And, the changes were more and more obvious by the time l ine. These changes were differentiable at 3 weeks after injection of ethanol, and became obvious at 6 weeks. These changes were more obvious at the part that near the injection canal. The changes in threefoot canine group were more obvious than that in four-foot canine group. Conclusion Resorption of necrotic compact bone trabecular may weaken the structural properties of the femoral head. Moreover, remodel ing and repairing process of necrotic bone trabecular may be hampered by constant biomechanical loading that presented in three-foot bearing canines, and thereby further weaken the structural properties of the femoral head. Biomechanical loading may be one of the critical reasons that lead to the collapse of femoral head.
【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.
