Taurine treatment protects against chronic nicotine-induced oxidative changes

Experiments have shown that chronic nicotine administration caused oxidative damage in various organs by increasing lipid peroxidation products and decreasing the activity of endogenous antioxidants. The aim of this study was to investigate the effects of taurine treatment on nicotine-induced oxidative changes in rat thoracic aorta and heart and to explore the possible mechanisms of action. Male Wistar albino rats (200-250 g) were injected with nicotine hydrogen bitartrate (0.6 mg/kg; i.p.) or saline for 21 days. Taurine was administered (50 mg/kg; i.p.) alone or along with nicotine injections. After decapitation, the thoracic aorta and heart tissues were excised. The aorta was used for in vitro contractility studies or stored along with the heart samples for the measurement of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and collagen content. Tissue samples were also examined histologically. Serum samples were stored for the measurement of MDA, GSH and lactate dehydrogenase (LDH) activity. Chronic nicotine treatment impaired both the contraction and relaxation responses of the aortic rings to phenylephrine and acetylcholine, respectively. It increased lipid peroxidation, MPO levels and tissue collagen content of both aorta and heart samples. Taurine supplementation to nicotine-treated animals reversed the contractile dysfunction and restored the endogenous GSH levels and decreased high lipid peroxidation and MPO activities in both tissues. These data suggest that taurine supplementation effectively attenuates the oxidative damage because of chronic nicotine administration possibly by its antioxidant effects.     

蛋白酶抑制剂对肝缺血-再灌注损伤的保护作用

目的：探讨蛋白酶抑制剂及中性粒细胞在肝缺血－再灌注损伤中的作用。方法：采用大鼠部分肝缺血－再灌注模型，将健康雄性SD大鼠32只随机分为4组，手术对照组（A组），肝缺血90分钟组（B组），肝缺血90分钟，再灌注120分钟组（C组），肝缺血90分钟，再灌注120分钟加缺血前30分钟静注乌司他丁组（D组），观察动物肝组织病理切片；分别测定血浆中天冬氨酸转氨酶（AST），丙氨酸转氨酶（ALT），乳酸脱氢酶（LDH）浓度，测定肝组织中髓过氧化物酶（MPO）含量，结果：光镜下B，C2组与A组比较，肝小叶结构紊乱，肝血窦和中央静脉有程度不同的淤血，有的肝血窦变窄，内皮细胞及肝细胞普遍水肿变性；C组肝细胞坏死较B组明显；D组上述改变明显减轻，血浆中肝功能酶学指标显著升高（B，C组与A组比较，P均＜0．05），肝组织中MPO活性升高，以再灌注120分钟组为著（C组与A组比较，P＜0．01），D组血浆中ALT，AST，LDH和MPO含量均较C组明显下降，结论：肝缺血－再灌注时，聚集，黏附在肝组织中的大量中性粒细胞通过释放蛋白酶造成肝损伤，蛋白酶抑制剂乌司他丁能明显减轻这种损伤，保护肝功能。     

复方片仔癀肝宝对酒精诱导的慢性肝损伤氧化应激的保护作用研究

目的:探讨复方片仔癀肝宝对酒精性肝病(Aleoholie Liver Disease,ALD)模型大鼠氧化应激的保护作用。方法:60只SPF级SD大鼠,随机分为正常对照组、模型组、阳性药对照组及肝宝低、中、高剂量组,每组10只。除正常对照组外其余各组用酒精联合高脂饲料喂养2周,造ALD模型,连续给药4周后取材。全自动生化仪检测血清中谷丙转氨酶(ALT)、谷草转氨酶(AST)、碱性磷酸酶(ALP)、乳酸脱氢酶(LDH)的含量变化;检测肝组织中超氧化物歧化酶(SOD)、丙二醛(MDA)和谷胱甘肽过氧化物酶(GSH-Px)的表达;HE染色,观察肝组织病理变化。结果 :模型组血清中ALT、AST、ALP、LDH的活性较正常对照组均有明显的上升,且肝组织中MDA水平明显上升,SOD、GSH-Px水平明显下降(P0.01)。与模型组相比,肝宝各组ALT、AST、ALP、LDH的活性及MDA水平明显降低,而SOD、GSH-Px水平明显上升(P0.05)。HE染色结果显示复方片仔癀肝宝不同剂量组对肝组织脂肪变性、肝内脂类聚集有明显的改善作用,并且存在剂量效应关系。结论:复方片仔癀肝宝能显著减轻酒精和高脂诱导的肝损伤,其机制可能与提高肝组织的抗氧化能力有关。     

橙皮苷通过抑制高迁移率族蛋白B1释放减轻对乙酰氨基酚致小鼠急性肝损伤

目的研究橙皮苷（HDN）对对乙酰氨基酚（APAP）诱导小鼠急性肝损伤的保护作用。方法48只雄性BALB／c小鼠随机均分为6组：正常组,模型组,HDN组（浓度分别为500、250、125mg／kg）,联苯双酯组。HDN组分别灌胃不同浓度的HDN悬液,联苯双酯组灌胃等量联苯双酯溶液,正常组和模型组给予等量的0．5％羧甲基纤维素钠溶液,各组1次／d,连续10d。末次灌胃后禁食不禁水,2h后除正常组外其余各组腹腔注射APAP（150mg／kg）溶液建立小鼠急性肝损伤动物模型。16h后处死小鼠,检测血清谷丙转氨酶（ALT）、谷草转氨酶（AST）及肝匀浆丙二醛（MDA）、谷胱甘肽（GSH）水平,光学显微镜下观察肝组织病理组织学变化,逆转录一聚合酶链式反应（RT—PCR）法和免疫组织化学法测定肝脏高迁移率族蛋白B1（HMGB1）水平。结果HDN能显著降低小鼠血清ALT、AST、肝匀浆MDA水平,提高肝组织中GSH活性,改善肝组织损伤程度。RT—PCR法和免疫组织化学法显示,HDN可以抑制HMGBl的转录和释放。结论HDN对APAP诱导小鼠急性肝损伤具有保护作用,可能与其抑制HMGBlmRNA转录和释放有关。     

Antithrombin III prevents 60 min warm intestinal ischemia reperfusion injury in rats

We investigated the effect of antithrombin III on 60 min warm intestinal ischemia-reperfusion (IR) injury in rats. Sprague-Dawley rats, weighing 220–250 g, were divided into three groups: group 1 sham-operated group (no IR injury, n=8), group 2 ischemic control group (control, Ringer’s lactate infused, n=8), group 3 Antithrombin III treated group (250 U/kg before ischemia, n=8). Intestinal ischemia was induced in rats by occluding the superior mesenteric artery for 60 min. Malondialdehyde (MDA) levels, myeloperoxi-dase activity (MPO) and mucosal damage were investigated after 120 min reperfusion. Elevated MDA levels and MPO activity and severe histopathological damage were observed in the control group compared with the sham group (P<0.05). Decreased MDA levels and MPO activity and less histopathological damage were detected in group 3 compared with the control group (P<0.05). Accumulation of lipid peroxidation products and neutrophils in mucosal tissues were significantly inhibited by antithrombin III treatment. We conclude that treatment with antithrombin III before intestinal ischemia prevents histological damage in rats.     

褪黑激素对严重烧伤早期肾功能损害的保护作用

目的观察褪黑激素（MLT）对严重烧伤大鼠肾组织氧化应激损伤和肾功能不全的保护作用及机制。方法将70只SD大鼠随机分为假手术组（10只）、烫伤组（用背部浸入沸水中30S造成30％总体表面积Ⅲ度烫伤模型，30只）和MLT治疗组（伤后立即腹腔注射MLT 10mg／kg，每12h补充注射1次，30只）。检测各组伤后6、24和72h肾组织丙二醛（MDA）和还原型谷胱甘肽（GSH）含量、血浆肌酐（BCr）及尿素氮（BUN）水平，以及伤后6h肾组织谷胱甘肽过氧化物酶（GSH-Px）和髓过氧化物酶（MPO）活性。结果烫伤后各时间点肾组织MDA水平明显升高，而GSH含量则显著下降，二者变化均以伤后6h最明显（P均〈0．01）。BCr及BUN水平在烧伤后6h达高峰（P均〈0．01），然后呈进行性下降。单次MLT治疗使伤后6h肾组织MDA水平降低27．8％（P〈0．01），使GSH含量提高44．4％（P〈0．05），并抑制BCr及BUN水平（P〈0．05和P〈0．01）。连续注射MLT对以上各指标均无明显影响。此外，MLT使烧伤后6h肾组织MPO水平降低30．2％（P〈0．05），但对GSH-Px活性无明显影响。结论30％Ⅲ度烫伤可导致大鼠肾脏发生明显的氧化应激损伤（伤后72h内）及急性肾功能不全（伤后24h内），单次MLT治疗对二者均具有一定的保护作用，可能与MLT具有强大的自由基清除能力及抑制中性粒细胞聚集有关。     

乌司他丁对大鼠肝缺血-再灌流损伤的保护作用

目的研究乌司他丁对肝缺血再灌流损伤的保护作用。方法将45只成年雄性SD大鼠随机分成3组:假手术对照组(A组)、肝缺血30min、再灌流90min组(B组)、缺血前30min静脉注射乌司他丁+肝缺血30min、再灌流90min组(C组)。分别测血浆中天冬氨酸转氨酶(AST)、丙氨酸转氨酶(ALT)、乳酸脱氨酶(LDH)浓度;测定肝组织中髓过氧化物酶(MPO)含量,并取肝组织作光镜及电镜观察。结果再灌流90min时C组的血浆ALT、AST、LDH值及肝组织MPO含量均低于B组(P<0.01),且C组的肝细胞显微、超微结构损害的改变较B组的轻。结论乌司他丁能抑制肝缺血再灌流时中性粒细胞在肝组织中的聚集,从而对大鼠肝缺血再灌流所致肝细胞的结构和功能损伤有保护作用。     

异氟醚对大鼠肝脏缺血-再灌注损伤期氧自由基及细胞间黏附分子-1表达的影响

目的探讨异氟醚通过抑制细胞间黏附分子（ICAM-1）表达参与减轻肝脏缺血-再灌注（IR）损伤的可能调节机制。方法 32只雌性SD大鼠分为4组。A组大鼠行腹腔注射1%戊巴比妥钠40 mg/kg麻醉,进行手术但不阻断入肝血流;B组1%戊巴比妥钠麻醉后行部分肝脏IR;C组大鼠仅接受1.0 MAC异氟醚吸入麻醉,不阻断血流;D组采用1.0 MAC异氟醚麻醉,建立肝脏IR模型。肝脏缺血60 min,再灌注3 h后取肝组织和血液标本,检测血清丙氨酸转氨酶（ALT）和天冬门氨酸转氨酶（AST）、肝组织ICAM-1和肝组织还原型谷胱甘肽（GSH）、脂质过氧化物丙二醛（MDA）和超氧化物歧化酶（SOD）含量。结果与戊巴比妥钠麻醉比较,采用异氟醚处理后明显降低血清ALT和AST的水平,再灌注肝组织内GSH、SOD含量明显高于而MDA含量降低,同时抑制肝组织ICAM-1的表达。结论异氟醚麻醉能够有效减轻肝脏IR损伤,抑制氧自由基的生成和释放,具体机制可能与抑制ICAM-1表达致使细胞内GSH含量增加密切相关。     

Protection against liver injuries induced by low-temperature preservation with ulinastatin]

OBJECTIVE: To study whether ulinastatin has a protective role in cold preservation of liver and its mechanism. METHODS: To study the role of ulinastatin in protection of liver after cold preservation, the isolated rat liver with perfused either with cold perfusion fluid or perfused with cold perfusion fluid with ulinastatin. Liver tissue was harvested at 0, 12 and 24 hours after cold perfusion, and morphological changes were examined, alanine aminotransferase (ALT), lactate dehydrogenase (LDH), thoperoxidase (MPO), malondialehyde (MDA) and superoxide dismutase (SOD) contents were also determined. RESULTS: ALT, LDH, MPO and MDA contents were significantly lower in ulinastatin group than those in the control group at 12 and 24 hours, and levels of ALT, LDH, MDA and MPO were increased along with prolongation of preservation time (all P<0.01), but SOD was higher in ulinastatin group than the control group and it was increased along with the prolongation of time (all P<0.01). Compared with ulinastatin group, the control group showed obvious pathological changes. CONCLUSION: Protective effect of UW solution used in clinic weakens gradually as cold preservation time is prolonged. Ulinastatin has protective effect on liver against cold preservation injury, and its effect is better than the simple UW solution. Its mechanism is related to inhibition of anti-oxidation and aggregation neutrophil's accumulation effect of ulinastatin.     

Dehydroepiandrosterone prevents oxidative injury in obstructive jaundice in rats

We investigated the effect of dehydroepiandrosterone (DHEA) on oxidative injury in obstructive jaundice using three groups of rats: sham-operated group; common bile duct (CBD) group--the CBD was ligated; and DHEA group--DHEA administration followed CBD ligation. Liver function tests were performed using blood samples, and malondialdehyde concentration (MDA), superoxide dismutase activities (SOD), glutathione peroxidase (GPx), and total glutathione (tGSH) concentrations were measured in liver tissue. Serum alkaline phosphatase, gamma-glutamyltransferase and alanine aminotransferase activity were significantly elevated in the CBD group compared with the other groups. Serum aspartate aminotransferase and total bilirubin were highest in the CBD group; the MDA concentration was higher in the CBD group than the sham group. There were no significant differences in GPx activity among the groups. SOD activity and tGSH concentration were significantly lower in the CBD group than the other groups. DHEA may protect hepatic tissue against oxidative injury in obstructive jaundice by decreasing MDA concentration and increasing SOD activity and tGSH concentration.     

Antithrombin III prevents 60 min warm intestinal ischemia reperfusion injury in rats

We investigated the effect of antithrombin III on 60 min warm intestinal ischemia-reperfusion (IR) injury in rats. Sprague-Dawley rats, weighing 220-250 g, were divided into three groups: group 1 sham-operated group (no IR injury, n=8), group 2 ischemic control group (control, Ringer's lactate infused, n=8), group 3 Antithrombin III treated group (250 U/kg before ischemia, n=8). Intestinal ischemia was induced in rats by occluding the superior mesenteric artery for 60 min. Malondialdehyde (MDA) levels, myeloperoxidase activity (MPO) and mucosal damage were investigated after 120 min reperfusion. Elevated MDA levels and MPO activity and severe histopathological damage were observed in the control group compared with the sham group (P<0.05). Decreased MDA levels and MPO activity and less histopathological damage were detected in group 3 compared with the control group (P<0.05). Accumulation of lipid peroxidation products and neutrophils in mucosal tissues were significantly inhibited by antithrombin III treatment. We conclude that treatment with antithrombin III before intestinal ischemia prevents histological damage in rats.     

Acute alcohol intoxication potentiates neutrophil-mediated intestinal tissue damage after burn injury

This study examined whether acute alcohol (EtOH) intoxication before burn injury potentiates postburn intestinal tissue damage and whether neutrophils have any role in the damage under those conditions. Male rats ( approximately 250 g) were gavaged with EtOH to achieve a blood EtOH level of approximately 100 mg/dL or with saline and received either approximately 12.5% or approximately 25% total body surface area (TBSA) burn or sham injury. Rats were killed at 4 or 24 h after injury, and various parameters were measured. As compared with sham animals, burn injury alone (regardless of size) resulted in a significant increase in intestinal tissue myeloperoxidase (MPO; an index of neutrophil infiltration) activity and IL-18 levels 4 h after injury. Furthermore, rats receiving 25% TBSA, but not 12.5%, burn exhibited intestine edema. The IL-18 and MPO activity were normalized at 24 h after injury in rats receiving 12.5% TBSA burn, whereas these parameters remained elevated at 24 h in rats with 25% burn. The presence of EtOH in rats at the time of burn injury exacerbated the levels of IL-18, MPO activity, and edema at 4 and 24 h after burn injury. Treatment of rats with anti-IL-18 antibodies or with antineutrophil antiserum prevented the increase in the above parameters after EtOH and burn injury, except that the depletion of neutrophils did not prevent the IL-18 increase. In summary, these findings suggest that acute EtOH intoxication exacerbates postburn intestinal tissue damage after burn injury, and that it is, in part, neutrophil mediated.     

Protective effect of taurine against alendronate-induced gastric damage in rats

Alendronate (ALD) causes serious gastrointestinal adverse effects. The aim of this study was to investigate whether taurine (TAU), a semi-essential amino acid and an antioxidant, improves the alendronate-induced gastric injury. Rats were administered 20 mg/kg ALD by gavage for 4 days, either alone or following treatment with TAU (50 mg/kg, i.p.). On the last day of treatment, following drug administration, pylorus ligation was performed and 2 h later, rats were killed and stomachs were removed. Gastric acidity and tissue ulcer index values, lipid peroxidation and glutathione (GSH) levels, myeloperoxidase (MPO) activity as well as the histologic appearance of the stomach tissues were determined. Chronic oral administration of ALD induced significant gastric damage, increasing lipid peroxidation, MPO activity and collagen content, as well as decreasing tissue GSH levels. Treatment with TAU prevented the damage and also the changes in biochemical parameters. Findings of the present study suggest that ALD induces oxidative gastric damage by a local irritant effect, and that TAU ameliorates this damage by its antioxidant and/or membrane-stabilizing effects.     

丙酮酸乙酯对烫伤延迟复苏大鼠多器官功能及死亡率的影响

目的观察丙酮酸乙酯（EP）对烫伤延迟复苏动物多器官功能及死亡率的影响，探讨其保护作用的机制。方法采用雄性Wistar大鼠30％总体表面积Ⅲ度烫伤模型。实验分为两部分进行：①死亡率观察：130只大鼠按照随机数字表法分为假烫伤组（n=10）、烫伤组（n=60。伤后6h腹腔注射生理盐水40ml／kg进行复苏，然后按照不同时间点腹腔注射等量生理盐水）和EP组（n=60。伤后6h腹腔注射生理盐水40ml／kg进行复苏，按不同时间点腹腔注射EP液40mg／kg。每日2次．间隔12h。给药3d）。除假烫伤组外，各组又分为伤前2h（n=20）、伤后2h（n=20）和伤后12h（n=20）给药3个亚组。观察不同时间点各组动物7d死亡率。②器官功能观察：70只大鼠随机分为假烫伤组（n=10）、烫伤组（n=30）和EP组（n=30，伤后2h给药），并分别于伤后12、24和72h活杀，检测器官功能指标改变。结果与烫伤组相比，伤后12hEP组动物死亡率显著降低（35．0％比75．0％，P〈0．05）。伤后2hEP组血清丙氨酸转氨酶、天冬氨酸转氨酶、尿素氯、肌酐、肌酸激酶水平及肺组织髓过氧化物酶活性均明显下降（P〈0．05或P〈0．01）。结论EP能明显改善严重烫伤延迟复苏大鼠的预后，并对重要器官功能具有显著保护作用。     

双歧三联活菌对硫代乙酰胺所致肝纤维化大鼠的预防作用及其机制的研究

目的 明确双歧三联活菌对硫代乙酰胺(TAA)诱导的大鼠肝纤维化形成是否具有预防作用,并探讨可能机制.方法 将30只SD大鼠随机分为正常对照组、模型组、预防组,每组10只.采用TAA皮下注射制备肝纤维化模型,预防组在此基础上同时给予双歧三联活菌制剂灌胃.检测内毒素、丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)、乳酸脱氢酶(LDH)和丙二醛(MDA).HE染色、天狼猩红染色观察肝组织形态学改变及胶原纤维沉积状况,免疫组织化学染色检测肝组织内毒素受体CD14的表达.结果 模型组肝损伤最重、胶原面积百分比明显高于正常对照组和预防组(P均<0.01).与模型组比较,预防组内毒素、ALT、AST、LDH和MDA水平均明显降低(P均<0.05),肝组织CD14阳性细胞表达明显减少(P<0.05).结论 双歧三联活菌可以预防TAA诱导的大鼠肝纤维化的形成,机制可能与其减轻肠源性内毒素血症,下调肝组织CD14的表达,减弱内毒素介导的继发性肝损伤有关.     

17β-estradiol attenuates reduced-size hepatic ischemia/reperfusion injury by inhibition apoptosis via mitochondrial pathway in rats

The aim of this study was to investigate the effect of 17β-estradiol (E2) on hepatocyte apoptosis after reduced-size hepatic ischemia/reperfusion (I/R) injury and its mechanism. A rat model of reduced-size hepatic I/R injury was established. Sprague-Dawley rats were randomly allocated into sham, I/R, and E2 + I/R group. 17β-Estradiol (4 mg/kg) or the vehicle was administered i.p. 1 h before ischemia and immediately after operation. For each group, 10 rats were used to investigate the survival during a week after reperfusion. Blood samples and liver tissues were obtained in the remaining animals after 3, 6, 12, and 24 h of reperfusion to assess serum aspartate aminotransferase and alanine aminotransferase levels, liver tissue malondialdehyde concentration, superoxide dismutase activity, and histopathologic changes. Apoptosis ratio; expression of cytochrome c, Bcl-2, and Bax proteins; and enzymatic activities of caspase 9 and caspase 3 were performed in the samples at 12 h after reperfusion. The serum aspartate aminotransferase and alanine aminotransferase levels and tissue malondialdehyde concentration were increased in the I/R group, whereas the increase was significantly reduced by E2. The superoxide dismutase activity, depressed by I/R injury, was elevated back to normal levels by treatment with E2. Severe hepatic damage was observed by light microscopy in the I/R group, whereas administration of E2 resulted in tissue and cellular preservation. Furthermore, E2 inhibited hepatocellular apoptosis by upregulating the ratio of Bcl-2 and Bax expression, reduced cytosolic cytochrome c level, and decreased caspase 9 and caspase 3 activities. The 7-day survival rate was significantly higher in the E2 + I/R group than in the I/R group. These results indicated that E2 protects liver tissues from reduced-size hepatic I/R injury by suppressing mitochondrial apoptotic pathways.     

Collagen glucosyltransferase activity in human serum

Collagen glucosyltransferase activity was demonstrated in human serum. The assay used for this enzyme was shown to be specific, whereas attempts to measure collagen galactosyltransferase activity were unsuccessful. It is suggested that most of the serum collagen glucosyltransferase activity originates from the extravascular tissue, although it is possible that some is derived from the platelets.The activity of collagen glucosyltransferase in serum varied somewhat with age, the mean value in newborn infants being about 30 per cent higher than the level in adult subjects.In a randomly selected group of 50 hospitalized patients with various diseases, serum collagen glucosyltransferase activity was found to be elevated in 12 cases. The activities of reference enzymes (mainly aspartate aminotransferase, alanine aminotransferase and alkaline phosphatase) were elevated in 10 of these 12 patients and in three additional patients within the group. However, collagen glucosyltransferase activity showed no clear linear correlation with the activities of the reference enzymes within this group of 15 patients with elevated enzyme activities, the correlation being highest in the case of aspartate aminotransferase activity (r = +0.56, P < 0.05). In two patients collagen glucosyltransferase activity was elevated but all reference enzyme activities were normal, this pattern being possibly caused by damage concentrated in the connective tissue.The measurement of collagen glucosyltransferase activity in serum may prove useful in studying destructive diseases affecting the collagen-producing tissues.     

抗氧化剂预防低血糖所致肌肉损伤的研究

目的 探讨低血糖状态下血浆和组织中谷胱甘肽含量的变化以及还原型谷胱甘肽（GSH）对血清酶活性的抑制作用。方法 静脉注射胰岛素诱发低血糖，并持续60min，然后输注葡萄糖解除低血糖。结果发现诱发低血糖后6h，血浆GTSH，氧化型谷胱甘肽（GSSG），谷胱甘肽总量（TGSH）及GSSG/TGSH比值均明显升高，肝脏GSH和TGSH明显减少，心肌和骨骼肌CSSG和GSSG/TGSH比值明显增高，同时伴有血清酶（ALT，AST，LDH，CK）活性升高，预先注射CSH后诱发低血糖组，血浆GSSG和GSSG/TGSH比值明显下降，并抑制了血清酶的活性。结论 低血糖所致的血清酶活性的升高与体内谷胱甘肽氧化还原状态的改变有关。补充抗氧化剂GSH可以预防低血糖所致的肌肉损伤。     

还原型谷胱甘肽对急性有机磷农药中毒肝功能损害的治疗

目的探讨还原型谷胱甘肽对急性有机磷农药中毒肝功能损害的治疗价值。方法将58例急性有机磷农药中毒伴肝功能损害的患者随机分为Ⅰ组和Ⅱ组。Ⅰ组加用还原型谷胱甘肽1.2g/d.qd.ivgtt,其余治疗两组相同。于治疗前后测定血清谷草转氨酶(AST)、谷丙转氨酶(ALT)、凝血酶原时间(PT)等,并观察临床病情。结果Ⅰ组AST、ALT、PT较Ⅱ组明显好转(P<0.01);Ⅰ组AST、ALT好转率较Ⅱ组高(P<0.05)。结论还原型谷甘肽对急性有机磷农药中毒肝功能损害具有较好的治疗作用。     

新型钙增敏剂哒嗪酮对低血容量性休克大鼠肝脏结构与功能的影响

目的：研究哒嗪酮（ＭＣＩ１５４）对低血容量性休克大鼠肝脏功能和结构改变的影响。方法：用大鼠低血容量性休克模型,设立ＭＣＩ１５４治疗组和生理盐水对照组,测定肝脏组织血流量以及肝脏组织提取液和线粒体悬液的生化指标,观察肝脏结构及超微结构的变化。结果：ＭＣＩ１５４治疗后肝脏组织血流量和Ｈ＋ＡＴＰ酶的活性显著高于相应的生理盐水对照组,组织提取液中丙氨酸转氨酶、乳酸脱氢酶、β葡萄糖醛酸酶和丙二醛以及线粒体内钙含量等指标显著低于相应的生理盐水对照组,肝脏细胞结构、超微结构损伤程度明显轻于生理盐水对照组。结论：ＭＣＩ１５４可显著增加大鼠肝脏组织血流量,减轻肝细胞损伤程度,延缓线粒体内钙超载进程,保护Ｈ＋ＡＴＰ酶的活性,对低血容量性休克大鼠肝脏结构和功能具有显著的保护作用。