Effects of acetylcysteine on micro-inflammation and pulmonary ventilation in chronic obstructive pulmonary disease exacerbation

BACKGROUND Acute exacerbation of chronic obstructive pulmonary disease(AECOPD)is a serious complication of chronic obstructive pulmonary disease,often characterized by increased morbidity and mortality.In traditional Chinese medicine,AECOPD is linked to phlegm-heat and blood-stasis,presenting symptoms like thick sputum,fever,and chest pain.It has been shown that acetylcysteine inhalation in conjunction with conventional therapy significantly reduced inflammatory markers and improved lung function parameters in patients with AECOPD,suggesting that acetylcysteine may be an important adjunctive therapy for patients with phlegm-heat-blood stasis type AECOPD.AIM To investigate the effect of acetylcysteine on microinflammation and lung ventilation in patients with phlegm-heat and blood-stasis-type AECOPD.METHODS One hundred patients with phlegm-heat and blood-stasis-type AECOPD were randomly assigned to two groups.The treatment group received acetylcysteine inhalation(10%solution,5 mL,twice daily)along with conventional therapy,whereas the control group received only conventional therapy.The treatment duration was 14 d.Inflammatory markers(C-reactive protein,interleukin-6,and tumor necrosis factor-alpha)in the serum and sputum as well as lung function parameters(forced expiratory volume in one second,forced vital capacity,and peak expiratory flow)were assessed pre-and post-treatment.Acetylcysteine inhalation led to significant reductions in inflammatory markers and improvements in lung function parameters compared to those in the control group(P<0.05).This suggests that acetylcysteine could serve as an effective adjunct therapy for patients with phlegm-heat and blood-stasis-type AECOPD.RESULTS Acetylcysteine inhalation significantly reduced inflammatory markers in the serum and sputum and improved lung ventilation function parameters in patients with phlegm-heat and blood-stasis type AECOPD compared with the control group.These differences were statistically significant(P<0.05).The study concluded that acetylcysteine inhalation had a positive effect on microinflammation and lung ventilation function in patients with this type of AECOPD,suggesting its potential as an adjuvant therapy for such cases.CONCLUSION Acetylcysteine inhalation demonstrated significant improvements in reducing inflammatory markers in the serum and sputum,as well as enhancing lung ventilation function parameters in patients with phlegm-heat and bloodstasis type AECOPD.These findings suggest that acetylcysteine could serve as a valuable adjuvant therapy for individuals with this specific type of AECOPD,offering benefits for managing microinflammation and optimizing lung function.

N-acetylcysteine inhibits activation of toll-like receptor 2 and 4 gene expression in the liver and lung after partial hepatic ischemia-reperfusion injury in mice

BACKGROUND: Toll-like receptor 2 and 4 (TLR2/4) may play important roles in ischemia-reperfusion (I/R) injury, and N-acetylcysteine (NAC) can prevent the generation of reactive oxygen species (ROS) induced by I/R injury. This study aimed to investigate the changes in TLR2/4 gene expression in the liver and lung after I/R injury with or without NAC pretreatment. METHODS: BALB/c mice were used in a model of partial hepatic I/R injury and randomly assigned to a sham-operated control group (SH), a hepatic ischemia/reperfusion group (I/R) or a NAC pretreated, hepatic I/R group (I/R-NAC). The levels of TNF-alpha in the portal vein and plasma alanine aminotransferase (ALT) were measured at 1 and 3 hours after reperfusion. The lung wet-to-dry ratio was measured, and the expression of TLR2/4 mRNA and protein in the liver and lung were assessed with RT-PCR and Western blotting at the same time points. RESULTS: Compared with the I/R group, the expression of TLR2/4 mRNA and protein in the liver and lung in the I/R-NAC group was decreased at the same time point (P<0.05). The levels of portal vein TNF-a and plasma ALT increased continuously in the l/R group at I and 3 hours of reperfusion compared with the SH group; however, they declined significantly in the group pretreated with NAC (P<0.05). The extent of lung edema was relieved in the I/R-NAC group compared with the I/R group (P<0.05). CONCLUSIONS: TLR2/4 was activated in the liver and lung in the process of partial hepatic I/R injury. NAC inhibited the activation of TLR2/4 and the induction of TNF-alpha resulting from I/R injury via modulating the redox state, thus it may mitigate liver and lung injury following partial hepatic I/R in mice.

N-acetylcysteine attenuates reactive-oxygen-speciesmediated endoplasmic reticulum stress during liver ischemia-reperfusion injury

AIM:To investigate the effects of N-acetylcysteine(NAC) on endoplasmic reticulum(ER) stress and tissue injury during liver ischemia reperfusion injury(IRI).METHODS:Mice were injected with NAC(300 mg/kg) intraperitoneally 2 h before ischemia.Real-time polymerase chain reaction and western blotting determined ER stress molecules(GRP78,ATF4 and CHOP).To analyze the role of NAC in reactive oxygen species(ROS)-mediated ER stress and apoptosis,lactate dehydrogenase(LDH) was examined in cultured hepatocytes treated by H2O2 or thapsigargin(TG).RESULTS:NAC treatment significantly reduced the level of ROS and attenuated ROS-induced liver injury after IRI,based on glutathione,malondialdehyde,serum alanine aminotransferase levels,and histopathology.ROS-mediated ER stress was significantly inhibited in NAC-treated mice.In addition,NAC treatment significantly reduced caspase-3 activity and apoptosis after reperfusion,which correlated with the protein expression of Bcl-2 and Bcl-xl.Similarly,NAC treatment significantly inhibited LDH release from hepatocytes treated by H2O2 or TG.CONCLUSION:This study provides new evidence for the protective effects of NAC treatment on hepatocytes during IRI.Through inhibition of ROS-mediated ER stress,NAC may be critical to inhibit the ER-stressrelated apoptosis pathway.

N-acetylcysteine treats intravenous amiodarone induced liver injury

We report a case of intravenous(IV) amiodarone drug induced liver injury(DILI).The patient received IV N-acetylcysteine(NAC) which resulted in a rapid improvement in liver enzymes.While the specific mechanisms for the pathogenesis of IV amiodaroneDILI and the therapeutic action of IV NAC are both unknown, this case strongly implies at least some commonality.Because IV amiodarone is indicated for the treatment of serious cardiac arrhythmias in an intensive care unit setting, some degree of ischemic hepatitis is likely a cofactor in most cases.

Neuroprotective effects of combined lead and cadmium,as well as N-acetylcysteine,on cerebral cortical neurons following lipid peroxidation injury

BACKGROUND： Studies have reported the antioxidant effects of lead and cadmium in the central nervous system, but very few have addressed the combined toxicity of lead and cadmium. The mechanisms by which these combined heavy metals are toxic, as well as how to protect cells from these agents, remains poorly understood. OBJECTIVE： Primary cultured rat cortical neurons were used to determine the effects of combined lead and cadmium on levels of glutathione peroxidase （GSH-Px）, superoxide dismutase （SOD）, catalase （CAT）, and acetylcholinesterase （ACHE）, as well as malondialdehyde （MDA）, and to evaluate the neuroprotective effects of N-acetylcysteine （NAC）. DESIGN, TIME AND SETTING An in vitro toxicological observation was performed at the Comparative Medicine Center of Yangzhou University from August 2007 to April 2008. MATERIALS： Lead acetate, cadmium acetate, and NAC were purchased from Sigma-Aldrich （St. Louis, USA）. Commercial kits of GSH-Px, SOD, CAT, ACHE, and MDA were purchased from Nanjing Jiancheng Bioengineering Institute, Nanjing, China. METHODS： The cerebral cortical neurons were isolated from newborn Sprague dawley rats at 24 hours after birth and primary cultured for 6 days. Thereafter, the cells were treated with a range of cadmium doses （0, 5.0, and 10.0μmol/L）, lead doses （0, 1.0, and 2.0 μmol/L）, or a combination of the two for 12 hours at 37℃in a 5% CO2 incubator, respectively. In addition, the cells were incubated with different doses of cadmium and/or lead and （0 and 50 μmol/L） NAC for 12 hours to assess the protective effects on cell survival. MAIN OUTCOME MEASURES： The activity of SOD, GSH-Px, CAT, and ACHE, as well as MDA content, in the cell lysates was detected using commercial kits. RESULTS： At 12 hours after treatment, compared to the control group, activity of GSH-Px, SOD, and AChE in the lead, cadmium, or combined treated cells was significantly decreased with increasing doses of cadmium/or lead （P 〈 0.05）, but CAT activity and MDA levels were significantly increased （P 〈 0.05）. The combination of cadmium and lead led to higher levels of toxicity than individual exposure. CONCLUSION： The degree of oxidative damage increased when the two heavy metals were combined. NAC protected neonatal cortical neurons by increasing activity of anti-oxidative enzymes and reducing lipid peroxidation, but the reduction was not statistically significant.

Split-dose or hybrid nonsteroidal anti-inflammatory drugs and Nacetylcysteine therapy for prevention of post-retrograde cholangiopancreatography pancreatitis

BACKGROUND Despite significant technical and training improvements, the incidence of postendoscopic retrograde cholangiopancreatography(ERCP) pancreatitis(PEP) has not significantly dropped. Although many studies have evaluated the efficacy of various agents, e.g. nonsteroidal anti-inflammatory drugs, octreotide,antioxidants, administered via various dosages, routes(oral, intrarectal or parenteral), and schedules(before or after the procedure), the results have been conflicting.AIM To evaluate efficacy of three pharmacologic prophylactic methods for prevention of PEP.METHODS In this prospective, single-center randomized trial, patients who underwent firsttime ERCP for choledocholithiasis were randomly assigned to three groups. The first group received 600 mg N-acetylcysteine 15 min prior to ERCP, and perrectum administration of 50 mg indomethacin both prior to and after completion of the ERCP. The second group was administered only the 50 mg indomethacin per-rectum both prior to and after the ERCP. The third group was administeredper-rectum 100 mg indomethacin only after the ERCP, representing the control group given the guideline-recommended regimen. The primary end-point was PEP prevention.RESULTS Among the total 211 patients evaluated during the study, 186 fulfilled the inclusion criteria and completed the protocol. The percentages of patients who developed PEP in each of the three groups were not significantly different(χ2 =2.793, P = 0.247). Among the acute PEP cases, for all groups, 14 patients developed mild pancreatitis(77.77%) and 4 moderate. No severe cases of PEP occurred, and in all PEP cases the resolution was favorable. No adverse events related to the medications(digestive hemorrhage, rectal irritation, or allergies)occurred.CONCLUSION The efficacies of split-dose indomethacin and combined administration(Nacetylcysteine with indomethacin) for preventing PEP were similar to that of the standard regimen.

Antimicrobial activity of alexidine alone and associated with N-acetylcysteine against Enterococcus faecalis biofilm

The purpose of this study was to assess the efficacy of alexidine（ALX）,alone and combined with N-acetylcysteine（NAC）,in eradicating two Enterococcus faecalis strain biofilms.The biofilms of E.faecalis ATCC 29212 and the clinical isolate E.faecalis D1 were grown in the MBEC-high-throughput device for 24 h and were exposed to five twofold dilutions of ALX（2%–0.007 8%）alone and combined with100 mg？mL21NAC,for 1 and 5 min.Eradication was defined as 100%kill of biofilm bacteria.The Student’s t-test was used to compare the efficacy of the associations of the two irrigants.After 1-min contact time,ALX eradicated the biofilms at all concentrations except for 0.007 8%and 0.015 6%–0.007 8%with E.faecalis ATCC 29212 and E.faecalis D1,respectively.Similar results for eradication and concentration were obtained when it was combined with 100 mg？mL21NAC.After 5 min of contact time,ALX alone and combined with NAC eradicated all enterococci biofilms.ALX showed antimicrobial properties against the two E.faecalis strain biofilms tested at very low concentrations,and its combined use with NAC was not seen to enhance its activity.

N-acetylcysteine amide protects against dexamethasone-induced cataract related changes in cultured rat lenses

Glucocorticoids (GCs) are one of the most widely used immunosuppressive and anti-inflammatory agents. However, their long term and systemic use is associated with adverse drug reactions including posterior subcapsular cataracts as one of its ocular complications. Balanced redox state is crucial for maintenance of lens transparency, and a high content of glutathione (GSH) in the lens is believed to play a key role in doing so. Depletion of GSH is implicated in the etiopathogenesis of dexamethasone-induced cataracts and, therefore, the present study was sought to evaluate the efficacy of a novel thiol antioxidant, N-acetylcysteine amide (NACA), in preventing dexamethasone-induced cataractogenesis. Cataract formation was induced by incubation of rat lenses with 5 μM dexamethasone. To assess whether NACA had a significant impact on dexamethasone-induced cataracts, the rat lenses were divided into four groups: 1) control group (Dulbecco’s Modified Eagle Medium (DMEM), 2) dexamethasone group (DMEM with 5 μM dexamethasone), 3) NACA-only group (50 μM NACA solution), and 4) NACA pretreatment group (50 μM NACA for 6 hours followed by 5 μM dexamethasone only for 18 hours). Lenses were cultured for 7 days at 37°C under 5% CO2. Lenses were evaluated daily using a dissecting microscope and photographed and graded for the development of opacity. The rat lenses in both the control and the NACA-only groups were clear, whereas all lenses within the dexamethasone-only group developed well-defined cataracts. Overall observations indicated that NACA inhibits cataract formation by limiting lipid peroxidation and increasing the ratio of GSH/GSSG in lens. Therefore, NACA can be developed into a potential adjunctive therapeutic option for patients undergoing therapy with GCs to inhibit glucocorticoid-induced cataracts.

N-acetylcysteine attenuates ischemia/reperfusion-induced cardiocyte apoptosis in diabetic rats

Objective：To study the effects of N-acetylcysteine （NAC） on ischemia/ reperfusion （I/R）-induced myocyte apoptosis in diabetic rats. Methods：The I/R heart model was made by ligation of the left anterior descending coronary artery （LAD） close to its origin. The LAD was occluded for 30 min followed by removal of ligation to allow subsequent reperfusion for 3 h. 72 rats were randomly divided into two groups , non-diabetic group （C, n = 36） and diabetic group ,（D, n = 36）. The animals in C group were randomly reassigned into sham-operated group （CS, n = 12） , I/R group （C I/R, n = 12） and treated with NAC group （CN, n = 12）. The rats in D group were also reassigned to sham-operated group （DS, n = 12） , I/R group （DI/R, n = 12） and treated with NAC group （DN, n = 12）. Malondialdehyde （MDA） and creatine kinase isoenzyme-MB （CK-MB） were measured. Infarct size（IS/AAR%）, the apoptosis index（AI） by TUNEL staining, the number of the cells positive for Caspase-3 and positive expression index （PEI） were calculated. Results：After I/R, the IS/AAR%, CK-MB, MDA, AI and Caspase-3 PEI were higher in diabetic group than those in non-diabetic group. Treatment with NAC decreased the above parameters in both non-diabetic and diabetic rats, but the parameters in diabetic rats were higher than those in non-diabetic rats. Conclusion：Diabetic rat hearts are more susceptible to I/R-induced myocardial necrosis and myocyte apoptosis. NAC can decrease the infarct size and attenuate cardiomyocyte apoptosis in both non-diabetic and diabetic rats, but the therapeutic effects are less effective in diabetic rats than those in non-diabetic rats.

N-acetylcysteine in acute pancreatitis

Premature trypsinogen activation and production of oxygen free radicals (OFR) are early pathogenic events which occur within acinar cells and trigger acute pancreatitis (AP). OFR exert their harmful effects on various cell components causing lipid peroxidation, disturbances in calcium homeostasis and DNA damage, which lead to increased cell injury and eventually cell death. This review presents the most recent data concerning the effects of N-Acetylcysteine (NAC), in the treatment of AP. NAC is an antioxidant capable of restoring the levels of Glutathione, the most important cellular antioxidant. Studies show the benef icial effects of NAC treatment in preventing OFR production and therefore attenuating oxidative damage. Additionally, NAC treatment has been shown to prevent the increase in cytosolic Ca2+ concentration and reduce the accumulation of enzymes in acinar cells during AP. The prevention, by NAC, of these pathological events occurring within acinar would contribute to reducing the severity of AP. NAC is also capable of reducing the activation of transcription factors especially sensitive to the cellular redox state, such as Nuclear factor-κB, signal transducer and activator of transcription-3 and mitogenactivated protein kinase. This leads to a down-regulation of cytokines, adhesion molecules and chemokine expression in various cell types during AP. These f indingspoint to NAC as a powerful therapeutic treatment, attenuating oxidative-stress-induced cell injury and other pathological events at early stages of AP, and potentially contributing to reducion in the severity of disease.

Efficacy of premedication with activated Dimethicone or N-acetylcysteine in improving visibility during upper endoscopy

AIM:To assess the efficacy of N-acetylcysteine(NAC) and activated Dimethicone in improving endoscopic mucosal visibility.METHODS:A total of 148 patients were randomly allocated into four groups to receive one of the following premedications:group A:100 mL water alone;group B:activated Dimethicone plus water(up to 100 mL);group C:NAC plus water(up to 100 mL);and group D:activated Dimethicone and NAC plus water(up to 100 mL).A single endoscopist blinded to the patients group assessed the gastric mucosal visibility scores(range 1-4) at four sites.The sum of the scores from the four sites was considered as the total mucosal visibility score(TMVS).RESULTS:The patients in group B showed a significantly lower TMVS than those of groups A and C(P < 0.001).The TMVS in patients of group D was significantly lower than that of groups A and C(P < 0.001).The TMVS did not significantly differ between groups B and D(P > 0.05).The difference between TMVS of groups C and A was not significant(P > 0.05).CONCLUSION:Premedication with activated Dimethicone 20 min prior to the upper endoscopy leads to the best visibility.NAC does not improve visualization by itself.

Premedication with pronase or N-acetylcysteine improves visibility during gastroendoscopy: An endoscopist-blinded, prospective, randomized study

AIM: To assess the efficacy of premedicaton with pronase or N-acetylcysteine (NAC) at 20 min before upper gastrointestinal (UGI) endoscopy and to determine whether pronase or NAC pretreatment influences the reliability of the rapid urease test. METHODS: A total of 146 patients were prospectively and randomly assigned into the study groups according to different premedications before endoscopy. One endoscopist assessed mucosal visibility (MV) with scores ranged from 1 to 4 at four sites in the stomach. The sum of the MV scores from these four locations was defined as the total mucosal visibility (TMV) score. Identification of H pylori was performed using CLO test, histology, and serology. RESULTS: The Group with pronase premedication had a significantly lower TMV score than did the groups with gascon and gascon water (P < 0.001 and P < 0.01, respectively). The group with NAC had a significantly lower TMV score than the group with gascon (P < 0.01) and a trend of a lower MV score than the group with gascon water (P = 0.06). The TMV score did not significantly differ between the group with pronase and the group with NAC (P = 0.39 and P = 0.14, respectively). The sensitivity and specificity of the CLO test were 92.5% and 93.9%, respectively, in groups premedicated with pronase and NAC together.CONCLUSION: Premedication with pronase or NAC at 20 min before UGI endoscopy improves the mucosal visibility of the stomach. Neither pronase nor NAC produces any obvious interference with the CLO test for the identification of H pylori infection.

N-acetylcysteine does not prevent post-endoscopic retrograde cholangiopancreatography hyperamylasemia and acute pancreatitis

瞄准：尖锐胰腺炎(AP ) 是最普通、经常严重的复杂并发症内视镜后退 cholangiopancreatography (ERCP ) 。在尖锐胰腺炎的致病的早步可能是毛状的内皮损害由导出氧的自由基调停了。N-acetylcysteine - 自由基 scavenger 可能在阻止尖锐胰腺炎和它是的 post-ERCP 是潜在地有效的也知道那个 N-acetylcysteine (ACC ) 罐头在 AP 的试验性的模型减少疾病的严厉。方法：106 个病人随机被分配到二个组。55 个病人被给 N-acetylcysteine (口头上地，在 ERCP 和 600 mg 前的 24 和 12 h 被给 iv 的二 600 mg 剂量，两次为在 ERCP 以后的二天的一天) 。控制组由被给 iv 的 51 个病人组成了。等渗盐两次为在 ERCP 以后的二天的一天。浆液和尿淀粉酶活动在过程以后在 ERCP 和 8 和 24 h 前被测量。主要结果参数是尖锐胰腺炎和第二等的结果参数是的 post-ERCP 在浆液和尿淀粉酶活动的组之间的差别。结果：处于在二个组之间的 post-ERCP 胰腺炎的率没有有效差量(10 病人外套， 4 在 ACC 组织， 6 在控制组织) 。也在在 ACC 组和控制组之间的基线和 post-ERCP 浆液和尿淀粉酶活动没有有效差量。结论：N-acetylcysteine 没能在 post-ERCP 胰腺炎上，以及在浆液和尿淀粉酶活动上表明任何重要预防效果。

Role of N-acetylcysteine in rifampicin-induced hepatic injury of young rats

瞄准：为了是学习 N-acetylcysteine (NAC ) 的角色，在 rifampicin (RMP ) 的一个保护的代理人导致了小老鼠的氧化肝的损害。方法：肝的损害被为 3 wk 给 RMP 的 50 mg/kg 体重生产。NAC (100 mg/kg 体重) 的剂量 intraperitoneally 与 RMP 在联合被给。类脂化合物的分析与体重，肝重量和组织学的观察一起在肝每氧化，巯基层次，细胞色素 P450，超级氧化物歧化酶(草皮) ，过氧化氢酶，谷胱甘肽过氧化物酶，还原酶和转移酶被估计。结果：当抗氧化的酶被改变时， RMP 暴露在身体和肝重量导致了没有变化但是非，蛋白质巯基(GSH ) 地位很好被保存。细胞色素 P450 系统并且每类脂化合物的氧化被 RMP 暴露导致。部分保护在肝对导致 RMP 的变化与 NAC 被观察，它在草皮和过氧化氢酶酶层次每氧化和减小从类脂化合物的增加的预防被证实。结论：NAC 保护小老鼠免于导致 RMP 的氧化肝的损害。

N-acetylcysteine attenuates alcohol-induced oxidative stess in rats

AIM: To investigate free-radical scavenger effect of nacetylcysteine in rats intragastrically fed with ethanol.METHODS: Twenty-four rats divided into three groups were fed with ethanol (6 g/kg/day, Group 1), ethanol and nacetylcysteine (1 g/kg, Group 2), or isocaloric dextrose (control group, Group 3) for 4 weeks. Then animals were sacrificed under ether anesthesia, and intracardiac blood and liver tissues were obtained. Measurements were made in both serum and homogenized liver tissues.Malondialdehyde (MDA) level was measured by TBARS method. Glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) levels were studied by commercial kits.Kruskal-Wallis test was used for statistical analysis.RESULTS: ALT and AST in Group 1 (154 U/L and 302 U/L,respectively) were higher than those in Group 2 (94 U/L and 155 U/L) and Group 3 (99 U/L and 168 U/L) (P=0.001for both). Serum and tissue levels of MDA in Group 1 (1.84nmol/mL and 96 nmol/100 mg-protein) were higher than that in Group 2 (0.91 nmol/mL and 64 nmol/100 mg protein)and Group 3 (0.94 nmol/mL and 49 nmol/100 mg-protein)(P＜0.001 for both). On the other hand, serum GSH-Px level in Group 1 (8.21 U/g Hb) was lower than that in Group 2(16 U/g Hb) and Group 3 (16 U/g-Hb) (P＜0.001). Serum and liver tissue levels of SOD in Group 1 (11 U/mL and 26U/100 mg-protein) were lower than that in Group 2 (18 U/mL and 60 U/100 mg protein) and Group 3 (20 U/mL and 60 U/100 mg-protein) (P＜0.001 for both).CONCLUSION: Ethanol-induced liver damage was associated with oxidative stress, and co-administration of n-acetylcysteine attenuates this damage effectively in rat model.

N-acetylcysteine attenuates oxidative stress and liver pathology in rats with non-alcoholic steatohepatitis

AIM: To evaluate attenuating properties of N-acetylcysteine (NAC) on oxidative stress and liver pathology in rats with non-alcoholic steatohepatitis (NASH). METHODS: Male Sprague-Dawley rats were randomly divided into three groups. Group 1 (control, n = 8) was free accessed to regular dry rat chow (RC) for 6 wk. Group 2 (NASH, n = 8) was fed with 100% fat diet for 6 wk. Group 3 (NASH + NAC20, n = 9) was fed with 100% fat diet plus 20 mg/kg per day of NAC orally for 6 wk. All rats were sacrificed to collect blood and liver samples at the end of the study. RESULTS: The levels of total glutathione (GSH) and hepatic malondialdehyde (MDA) were increased significantly in the NASH group as compared with the control group (GSH; 2066.7 ± 93.2 vs 1337.5 ± 31.5 μmol/L and MDA; 209.9± 43.9 vs 3.8 ±1.7 μmol/g protein, respectively, P < 0.05). Liver histopathology from group 2 showed moderate to severe macrovesicular steatosis, hepatocyte ballooning, and necroinflammation. NAC treatment improved the level of GSH (1394.8 ± 81.2 μmol/L, P < 0.05), it did not affect MDA (150.1 ± 27.0 μmol/g protein), but led to a decrease in fat deposition and necroinflammation. CONCLUSION: NAC treatment could attenuate oxidative stress and improve liver histology in rats with NASH.

N-acetylcysteine attenuates alcohol-induced oxidative stress in the rat

AIM: There is increasing evidence that alcohol-induced liverdamage may be associated with increased oxidative stress.We aimed to investigate free-radical scavenger effect of n-acetylcysteine in rats intragastrically fed with ethanol.METHODS: Twenty-four rats divided into three groups werefed with ethanol (6 g/kg/day, Group 1), ethanol and n-acetylcysteine (1 g/kg, Group 2), or isocaloric dextrose(control group, Group 3) for 4 weeks. Then animals weresacrificed under ether anesthesia, intracardiac blood andliver tissues were obtained. Measurements were performedboth in serum and in homogenized liver tissues.Malondialdehyde (MDA) level was measured by TBARSmethod. Glutathione peroxidase (GSH-Px) and superoxidedismutase (SOD) levels were studied by commercial kits.Kruskal-Wallis test was used for statistical analysis.RESULTS: ALT and AST in Group 1 (154 U/Land 302 U/L,respectively) were higher than those in Group 2 (94 U/L and155 U/L) and Group 3 (99 U/L and 168 U/L) (P＝0.001 forboth). Serum and tissue levels of MDA in Group 1 (1.84 nmol/mL and 96 nmol/100 mg-protein) were higher than Group 2(0.91 nmol/mL and 64 nmol/100 mg-protein) and Group 3(0.94 nmol/mL and 49 nmol/100 mg-protein) (P＜0.001 forboth). On the other hand, serum GSH-Px level in Group 1(8.21 U/g-Hb) was lower than Group 2 (16 U/g-Hb) andGroup 3 (16 U/g-Hb) (P＜0.001). Serum and liver tissue levelsof SOD in Group 1 (11 U/mL and 26 U/100 mg-protein)were lower than Group 2 (18 U/mL and 60 U/100 mg-protein)and Group 3 (20 U/mL and 60 U/100 mg-protein) (P＜0.001for both).CONCLUSION: This study demonstrated that ethanol-induced liver damage is associated with oxidative stress,and co-administration of n-acetylcysteine attenuates thisdamage effectively in rat model.

N-acetylcysteine protect lymphocytes and cytokines against heavy ion irradiation via counteracting the glutamate

We evaluated the protective effect of N-acetylcysteine (NAC) on immunity system irradiated by 12C6+ ion beam. Kun-Ming mice were whole-body irradiated by 12C6+ ion at doses of 0, 0.5, 1, 1.5, 2, 2.5 and 3 Gy. The results showed that in saline group, the lymphocytes DNA double-strand breaks (DSBs), maleic dialdehyde, thymocytes number in G 0 /G 1 and apoptosis percentage increased with dose increment, and the levels of interferon-γ, glutathione, superoxide radical (SOD) and natural killer cells activity decreased with dose increment. However, there were no significant changes in NAC-treated group. The data indicated that pre-treatment with NAC could significantly remove the ROS by counteracting the glutamate, decrease excessive lipid peroxidation reaction and SOD damages, and protect DNA, lymphocytes and cytokines against irradiation.

Oral administration of S-nitroso-N-acetylcysteine prevents the onset of non alcoholic fatty liver disease in rats

瞄准：在一个动物模型在不含酒精的脂肝疾病(NAFLD ) 的预防每氧化和口头的 SNAC 管理的效果在类脂化合物的抑制评估 S-nitroso-N-acetylcysteine (SNAC ) 的潜力。方法：NAFLD 被胆碱缺乏的饮食为 4 wk 在 Wistar 雄的老鼠导致。对待 SNAC 的动物(n=6 )(1.4 mg/kg 每 SNAC 的天，口头上地) 与 2 个控制组相比：(n=6 ) 收到了 PBS 答案，其它(n=6 ) 收到了 NAC 答案(7 mg/kg 每天) 。组织学的变量半关于宏和 microvacuolar 脂肪被测定变化，它的带的分发，坏死的 foci，门和 perivenular 纤维变性，并且煽动性与带的分发渗入。从肝 homogenates 的样品的 LOOH 被 HPLC 确定。在门静脉的血浆的硝酸盐层次被化合光估计。水的低密度的脂蛋白(LDL ) 暂停(200 microg protein/mL ) 在 37 度摄氏为 15 h 在 SNAC (300 micromol/L ) 的缺席和存在与 CuCl (2 )(300 micromol/L ) 被孵化。LDL 氧化的程度被 fluorimetry 估计。亚油酸(LA )(18.8 micromol/L ) 氧化被大豆 lipoxygenase (SLO )(0.056 micromol/L ) 当面在 37 度摄氏导致并且 N-acetylcysteine (NAC ) 和 SNAC (56 和 560 micromol/L ) 的缺席并且在 234 点监视了 nm。结果：在控制组的动物在仙子门区域开发了中等的宏和微小囊的丰满的变化。对待 SNAC 的动物与丰满的变化的缺席显示了仅仅分离的组织学的改变并且没得肝脂肪变性。在对待 SNAC 的组的 NAFLD 的缺席断然在肝匀浆在 LOOH 的集中与减少被相关，与控制组相比(0.7+/-0.2 nmol/mg 对 3.2+/-0.4 nmol/mg 蛋白质，分别地 P【0.05 ) ，当 aminotransferases 的浆液层次是未改变的时。在每氧化阻止类脂化合物的 SNAC 的能力作为模型底层用 LA 和 LDL 在在试管内实验被证实。结论：SNAC 的口服在用胆碱缺乏的饮食喂的 Wistar 老鼠阻止 NAFLD 的发作。这效果与 SNAC 的能力被相关每氧化在试管内和在试管内堵住类脂化合物的繁殖。

N-乙酰半胱氨酸联合缺血后处理减轻糖尿病小鼠心肌缺血再灌注后肺损伤的作用研究

目的研究N-乙酰半胱氨酸(NAC)联合缺血后处理(IPostC)对糖尿病小鼠心肌缺血再灌注后肺损伤的作用。方法选择15周龄雄性db/db糖尿病小鼠30只,分为假手术组(D-SO组,n=10)、心肌缺血/再灌注组(D-I/R组,n=10)和NAC联合缺血后处理组(D-NAC+IPostC组,n=10)。D-SO组小鼠开胸后不做任何处理;D-I/R组小鼠干预为冠状动脉左前降支结扎60 min,后复灌15 min。D-NAC+IPostC组在结扎冠状动脉左前降支前30 min腹腔注射NAC150 mg/kg,缺血后处理的干预方式为小鼠缺血60 min后即刻进行3个周期再灌注/缺血,然后再灌注15 min。于再灌注结束后颈动脉取血,检测血清C反应蛋白(CRP)、肿瘤坏死因子-α(TNF-α)、单核细胞趋化蛋白-1(MCP-1)水平,处死小鼠,取肺组织,检测湿干重(W/D)比值,光镜下观察肺组织病理形态学变化,计算肺损伤评分,测定肺组织氧化应激相关标志物谷胱甘肽(GSH)、超氧化物歧化酶(SOD)及丙二醛(MDA)水平,采用Western Blot法检测肺组织缺氧诱导因子1α(HIF-1α)和血管内皮生长因子(VEGF)的表达水平。结果与D-SO组比较,D-I/R组小鼠光镜下病理学损伤严重(P<0.05),肺W/D比值增加(P<0.05),血清TNF-α、CRP水平降低(P<0.05),MCP-1水平升高(P<0.05),肺组织MDA含量增加(P<0.05),SOD及GSH活性降低(P<0.05),肺组织HIF-1α及VEGF表达上调(P<0.05)。与D-I/R组比较,D-NAC+IPostC组肺组织镜下病理学损伤明显减轻(P<0.05),肺W/D比值降低(P<0.05),血清TNF-α、MCP-1水平降低(P<0.05),CRP水平升高(P<0.05),肺组织氧化应激因子MDA含量降低(P<0.05),抗氧化应激因子SOD及GSH活性升高(P<0.05),肺组织HIF-1α、血管内皮生长因子(VEGF)水平表达增高(P<0.05)。结论NAC联合IPostC可减轻糖尿病心肌缺血再灌注小鼠肺损伤,其机制可能与HIF-1α/VEGF信号通路相关。