乙酰半胱氨酸泡腾片联合噻托溴铵治疗慢性阻塞性肺疾病

目的:分析N–乙酰半胱氨酸泡腾片联合噻托溴铵治疗慢性阻塞性肺病的临床效果。方法:选取沙洋县人民医院2014年8月至2015年11月期间收治的50例慢性阻塞性肺疾病患者进行研究,随机将患者分为观察组和对照组,每组25例。两组患者均给予噻托溴铵治疗,观察组则在治疗中加入N–乙酰半胱氨酸泡腾片,比较两组患者的治疗效果。结果:观察组患者治疗后呼吸困难评分(MMRC)以及肺功能指标[1秒用力呼气容积(FEV1)、1秒用力呼气容积占预计值百分数(FEV1%pred)]均明显优于对照组,差异具有统计学意义(P <0.05);两组患者治疗期间的不良反应发生率比较,差异无统计学意义(P> 0.05)。结论:N–乙酰半胱氨酸泡腾片联合噻托溴铵治疗慢性阻塞性肺疾病整体效果显著。

PREPARATION AND CHARACTERIZATION OF WATER-SOLUBLE NEAR-INFRARED EMITTING PbS QUANTUM DOTS

A new facile method for preparing water-soluble near-infrared （NIR）-emitting PbS quantum dots （QDs） is proposed by using N-acetyl-L-cysteine （NAC, a derivate of L-cysteine） as its stabilizer. The influence of the precursor Pb/S molar ratio, the Pb/NAC molar ratio, and the pH of original solution on optical properties is explored. Results show that aqueous PbS QDs with strong NIR fluorescence can be prepared and their photoluminescence emission peaks can be tuned from 895 nm to 970 nm. Studies indicate that such aqueous QDs have a potential application in biomedical imaging, especially in noninvasive in vivo fluorescence imaging. In addition, the resulting PbS QDs are further characterized by a transmission electron microscopy and X-ray diffraction analysis.

NAC联合SM/FP治疗稳定期慢性阻塞性肺疾病的效果

目的:分析N–乙酰半胱氨酸(NAC)联合沙美特罗替卡松粉吸入剂(SM/FP)治疗稳定期慢性阻塞性肺疾病(S–COPD)的效果。方法:入选对象为2016年1月至2017年11月丰都县中医院收治的107例S–COPD患者,分为对照组53例和观察组54例。单用NAC治疗对照组,联合NAC与SM/FP治疗观察组。结果:对照组、观察组的有效率分别为69.81%、88.89%,观察组有效率显著高于对照组,差异具有统计学意义(P <0.05)。结论:联合SM/FP与NAC治疗S–COPD能提高疗效。

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 attenuates alcohol-induced oxidative stess in rats

AIM:To investigate free-radical scavenger effect of n- acetylcysteine 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 n- acetylcysteine (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=0.001 for both).Serum and tissue levels of MDA in Group 1 (1.84 nmol/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 26 U/100 rag-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 rag-protein) (P<0.001 for both). CONCLUSION:Ethanol-induced liver damage was associated with oxidative stress,and co-administration of n-acetylolsteine attenuates this damage effectively in rat model.

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

AIM： Acute pancreatitis （AP） is the most common and often severe complication of endoscopic retrograde cholangiopancreatography （ERCP）. The early step in the pathogenesis of acute pancreatitis is probably the capillary endothelial injury mediated by oxygen-derived free radicals. N-acetylcysteine - a free radical scavenger may be potentially effective in preventing post-ERCP acute pancreatitis and it is also known that N-acetylcysteine （ACC） can reduce the severity of disease in experimental model of AP. METHODS： One hundred and six patients were randomly allocated to two groups. Fifty-five patients were given N-acetylcysteine （two 600 mg doses orally 24 and 12 h before ERCP and 600 mg was given iv, twice a day for two days after the ERCP）. The control group consisted of 51 patients who were given iv. isotonic saline twice a day for two days after the ERCP. Serum and urine amylase activities were measured before ERCP and 8 and 24 h after the procedure. The primary outcome parameter was post-ERCP acute pancreatitis and the secondary outcome parameters were differences between groups in serum and urine amylase activity. RESULTS： There were no significant differences in the rate of post-ERCP pancreatitis between two groups （10 patients overall, 4 in the ACC group and 6 in the controlgroup）. There were also no significant differences in baseline and post-ERCP serum and urine amylase activity between ACC group and control group. CONCLUSION： N-acetylcysteine fails to demonstrate any significant preventive effect on post-ERCP pancreatitis, as well as on serum and urine amylase activity.

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

AIM, To study the role of N-acetylcysteine （NAC） as a protective agent in rifampicin （RMP）-induced oxidative hepatic injury of young rats. METHODS： Hepatic injury was produced by giving 50mg/kg body weight/day of RMP for 3 wk. A dose of NAC （100mg/kg body weight/day） was given in combination with RMP intraperitoneally. Analysis of lipid peroxidation, thiol levels, cytochrome P4se, superoxide dismutase （SOD）, catalase, glutathione peroxidase, reductase and transferase were estimated in liver along with the body weight, liver weight and histological observations. RESULTS： RMP exposure resulted in no change in body and liver weight while antioxidative enzymes were altered but the non protein thiol （GSH） status was well preserved. Cytochrome P450 system and peroxidation of lipids were induced by RMP exposure. Partial protection was observed with NAC against RMP-induced changes in liver, which was evidenced from the prevention of increase in lipid peroxidation and the reduction in SOD and catalase enzyme levels. CONCLUSION. NAC protects young rats against RMP- induced oxidative hepatic injury.

N-acetyl cysteine therapy in acute viral hepatitis

AIM: To investigate the effect of N-acetyl cysteine (NAC)on acute viral hepatitis (AVH).METHODS: We administered 200 mg oral NAC three times daily (600 mg/day) to the study group and placebo capsules to the control group. All patients were hospitalized and diagnosed as AVH. Blood total and direct bilirubin, ALT, AST,alkaline phosphatese, albumin and globulin levels of each patient were measured twice weekly until total bilirubin level dropped under 2 mg/dl, ALT level under 100 U/L, follow up was continued and then the patients were discharged.RESULTS: A total of 41(13 female and 28 male) AVH patients were included in our study. The period for normalization of ALT and total bilirubin in the study group was 19.7±6.9 days and 13.7±8.5 days respectively. In the control group it was 20.4±6.5 days and 16.9±7.8 days respectively (P＞0.05).CONCLUSION: NAC administration effected neither the time necessary for normalization of ALT and total bilirubin values nor duration of hospitalization, so we could not suggest NAC for the treatment of icteric AVH cases. However, our results have shown that this drug is not harmful to patients with AVH.

N-acetyl-L-cysteine combined with mesalamine in the treatment of ulcerative colitis: Randomized,placebo-controlled pilot study

AIM: To evaluate the effectiveness and safety of oral N-acetyl-L-cysteine (NAC) co-administration with mesalamine in ulcerative colitis (UC) patients. METHODS: Thirty seven patients with mild to moderate UC were randomized to receive a four-wk course of oral mesalamine (2.4 g/d) plus N-acetyl-L-cysteine (0.8 g/d) (group A) or mesalamine plus placebo (group B). Patients were monitored using the Modified Truelove-Witts Severity Index (MTWSI). The primary endpoint was clinical remission (MTWSI ≤ 2) at 4 wk. Secondary endpoints were clinical response (defined as a reduction from baseline in the MTWSI of ≥ 2 points) and drug safety. The serum TNF-α, interleukin-6, interleukin-8 and MCP-1 were evaluated at baseline and at 4 wk of treatment. RESULTS: Analysis per-protocol criteria showed clinical remission rates of 63% and 50% after 4 wk treatment with mesalamine plus N-acetyl-L-cysteine (group A) and mesalamine plus placebo (group B) respectively (OR = 1.71; 95% CI: 0.46 to 6.36; P = 0.19; NNT = 7.7). Analysis of variance (ANOVA) of data indicated a significant reduction of MTWSI in group A (P = 0.046) with respect to basal condition without significant changes in the group B (P = 0.735) during treatment. Clinical responses were 66% (group A) vs 44% (group B) after 4 wk of treatment (OR = 2.5; 95% CI: 0.64 to 9.65; P = 0.11; NNT = 4.5). Clinical improvement in group A correlated with a decrease of IL-8 and MCP-1. Rates of adverse events did not differ significantly between both groups. CONCLUSION: In group A (oral NAC combined with mesalamine) contrarily to group B (mesalamine alone), the clinical improvement correlates with a decrease of chemokines such as MCP-1 and IL-8. NAC addition not produced any side effects.

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

AIM： To evaluate the potential of S-nitroso-N-acetylcysteine （SNAC） in inhibition of lipid peroxidation and the effect of oral SNAC administration in the prevention of nonalcoholic fatty liver disease （NAFLD） in an animal model.METHODS： NAFLD was induced in Wistar male rats by choline-deficient diet for 4 wk. SNAC-treated animals （n=6） （1.4 mg/kg/day of SNAC, orally） were compared to 2 control groups： one （n=6） received PBS solution and the other （n=6） received NAC solution （7 mg/kg/d）. Histological variables were semiquantitated with respect to macro and microvacuolar fat changes, its zonal distribution, foci of necrosis, portal and perivenular fibrosis, and inflammatory infiltrate with zonal distribution. LOOHs from samples of liver homogenates were quantified by HPLC. Nitrate levels in plasma of portal vein were assessed by chemiluminescence. Aqueous low-density lipoprotein （LDL） suspensions （200 pg protein/mL） were incubated with CuCl2 （300 μmol/L） in the absence and presence of SNAC （300 μmol/L） for 15 h at 37 ℃ Extent of LDL oxidation was assessed by fluorimetry. Linoleic acid （LA） （18.8 μmol/L） oxidation was induced by soybean lipoxygenase （SLO） （0.056 μmol/L） at 37 ℃ in the presence and absence of N-acetylcysteine （NAC） and SNAC （56 and 560 pmol/L） and monitored at 234 nm. RESULTS： Animals in the control group developed moderate macro and microvesicular fatty changes in periportal area. SNAC-treated animals displayed only discrete histological alterations with absence of fatty changes and did not develop liver steatosis. The absence of NAFLD in the SNAC-treated group was positively correlated with a decrease in the concentration of LOOH in liver homogenate, compared to the control group （0.7±0.2 nmol/mg vs 3.2±0.4 nmol/mg protein, respectively, P〈0.05）, while serum levels of aminotransferases were unaltered. The ability of SNAC in preventing lipid peroxidation was confirmed in in vitro experiments using LA and LDL as model substrates. CONCLUSION： Oral administration of SNAC prevents the onset of NAFLD in Wistar rats fed with cholinedeficient diet. This effect is correlated with the ability of SNAC to block the propagation of lipid peroxidation in vitro and in vitro.

A novel manganese complex LMnAc selectively kills cancer cells by induction of ROS-triggered and mitochondrial-mediated cell death

We previously identified a novel synthesized metal compound, LMnAc （[L2Mn2（Ac）（H20）e]（Ac） （L=bis（2-pyridylmethyl） amino-2-propionic acid））. This compound exhibited significant inhibition on cancer cell proliferation and was more selective against cancer cells than was the popular chemotherapeutic reagent cisplatin. In this study, we further investigated the underlying molecular mechanisms of LMnAc-induced cancer cell death. We found that LMnAc achieved its selectivity against cancer cells through the transferrin-transferrin receptor system, which is highly expressed in tumor cells. LMnAc triggered cancer cells to commit autophagy and apoptosis, which was mediated by the mitochondrial pathway. Moreover, LMnAc disrupted mitochondrial function, resulting in mitochondrial membrane potential collapse and ATP reduction. In addition, LMnAc induced intracellular Ca^2＋ overload and reactive oxygen species generation. Interestingly, its anticancer effect was significantly reduced following pretreatment with the antioxidant N-acetyl cysteine, indicating that reactive oxygen species triggered cell death. Altogether, our data suggest that LMnAc appears to be a selectively promising anticancer drug candidate.

Chaetocin reactivates the lytic replication of Epstein-Barr virus from latency via reactive oxygen species

Oxidative stress, regarded as a negative effect of free radicals in vivo, takes place when organisms suffer from harmful stimuli. Some viruses can induce the release of reactive oxygen species （ROS） in infected cells, which may be closely related with their pathogenicity. In this report, chaetocin, a fimgal metabolite reported to have antimicrobial and cytostatic activity, was studied for its effect on the activation of latent Epstein-Barr virus （EBV） in B95-8 cells. We found that chaetocin remarkably up-regulated EBV lytic transcription and DNA replication at a low concentration （50 nmol L-l）. The activation of latent EBV was accompanied by an increased cellular ROS level. N-acetyl-L-cysteine （NAC）, an ROS inhibitor, suppressed chaetocin-induced EBV activation. Chaetocin had little effect on histone H3K9 methylation, while NAC also significantly reduced H3K9 methylation. These results suggested that chaetocin reactivates latent EBV primarily via ROS pathways.

Mycetismus:a review

Although rare,death from amanitin exposure poses a significant health risk and a diagnostic challenge to the clinician due to its rarity.This is one of the few conditions to be voluntarily reported by healthcare professionals.No antidote exists for this poisoning and,perhaps due to its rarity or lack of attention,the United States has lagged behind Europe for almost three decades in treatment,diagnostics and experimentation.This regrettable fact warrants the formation of a centralized agency for education,the advancement of research and the collection of data,to provide better treatment for the population.