N-乙酰半胱氨酸治疗特发性肺间质纤维化的临床研究

目的 探讨N-乙酰半胱氨酸治疗特发性肺间质纤维化( IPF)的效果.方法 将40例患者随机分为试验组和对照组,每组20例,试验组在口服常规激素治疗基础上加用N-乙酰半胱氨酸600 mg,3次/d口服,疗程12个月.观察两组临床症状及肺功能.结果 与对照组比较,试验组临床症状、肺功能明显改善.结论 对于IPF患者,强的松...     

吸入用乙酰半胱氨酸联合布地奈德 对小儿支气管肺炎的疗效

〔摘 要〕 目的：研究吸入用乙酰半胱氨酸联合布地奈德治疗支气管肺炎患儿的临床疗效。 方法：选取 2019 年 3 月至 2021 年 3 月厦门市海沧医院收治的支气管肺炎患儿 370 例，随机数字表法将其分为对照组、观察组，各 185 例。对照组给予 0.9 % 氯化钠注射液＋布地奈德雾化吸入治疗，观察组在对照组基础上联合吸入用乙酰半胱氨酸治疗。比较两组患儿疗效、 临床症状消失时间、免疫功能指标〔免疫球蛋白 A（IgA）、IgG、IgM〕和不良反应发生率。 结果：观察组患儿治疗总有 效率为 92.43 %，高于对照组的 71.35 %，差异具有统计学意义（P ＜ 0.05）；观察组患儿临床症状消失时间均显著短于对 照组，差异具有统计学意义（P ＜ 0.05）；治疗后，观察组患儿 IgA、IgG、IgM 水平均高于对照组，差异具有统计学意义 （P ＜ 0.05）；观察组患儿不良反应发生率为 3.24 %，低于对照组的 9.73 %，差异具有统计学意义（P ＜ 0.05）。 结论：吸入用乙酰半胱氨酸联合布地奈德雾化吸入治疗小儿支气管肺炎疗效确切，可提高治疗总有效率，缩短临床症状消退时间， 改善免疫功能水平，且安全性高，优于单纯使用布地奈德。     

N-乙酰半胱氨酸对糖尿病大鼠心肌NADPH氧化酶和eNOS表达的影响

目的探讨N-乙酰半胱氨酸(NAC)对糖尿病大鼠心肌NADPH氧化酶和内皮一氧化氮合酶(eNOS)表达的影响。方法大鼠随机分为正常对照组、正常对照组NAC治疗组、糖尿病组和糖尿病NAC治疗组。观察8周后测定心肌p22-phox和eNOS蛋白表达水平、血浆和心肌硝酸盐和亚硝酸盐(NOx)水平、血浆总抗氧化物浓度、心肌细胞横截面积和心肌超氧阴离子[O(2-)]水平。结果糖尿病大鼠8周时出现心重/体重和心肌细胞横截面积增加,心肌p22-phox蛋白表达和O(2-)水平显著升高,血浆总抗氧化物浓度降低,心肌eNOS蛋白表达、血浆和心肌NOx水平显著降低。NAC治疗8周能显著逆转糖尿病大鼠上述除心肌NOx外其他各项指标的变化。结论NAC能显著降低糖尿病大鼠心肌氧化应激水平,升高心肌eNOS水平,减轻氧化应激对心肌组织的损伤,产生心脏保护作用。     

乙酰半胱氨酸佐治小儿肺炎的效果评价

目的：研究乙酰半胱氨酸佐治小儿肺炎的临床效果。方法选取本院2013年10月~2014年10月收治的78例肺炎患儿,根据数字随机分组法原则,将患儿分为两组,每组各39例。对照组采用常规治疗,观察组在常规治疗基础上给予乙酰半胱氨酸治疗,比较两组的治疗效果、肺部啰音减少时间、咳嗽(咳痰)时间。结果观察组的总有效率为97.44%,高于对照组的82.05%(P<0.05);观察组的肺部啰音减少时间、咳嗽(咳痰)时间均短于对照组(P<0.05)。结论在常规治疗基础上加用乙酰半胱氨酸治疗小儿肺炎可以缩短患儿的肺部啰音减少时间、咳嗽(咳痰)时间,效果确切,值得临床推广应用。     

慢性间歇低氧大鼠氧化应激相关途径及抗氧化剂干预效果分析

目的 研究探讨慢性间歇低氧(CIH)大鼠氧化应激与血压及肾素-血管紧张素系统(RAS)相关性及N-乙酰半胱氨酸(NAC)对CIH相关性高血压的防治作用及机制.方法 24只SD雄性大鼠按随机数字表法分为CIH1、CIH2、CIH3和对照组,每组6只.CIH组大鼠循环给予氮气和压缩空气(每循环180 s,舱内最低氧浓度达6%～8%,维持20～25 s,然后恢复至21%,7 h/d),对照组大鼠常规饲养.CIH1组给予NAC 800 ml·kg-1·d-1腹腔注射,CIH2组予生理盐水5 ml·kg-1·d-1腹腔注射.结果第6周时CIH2、CIH3组大鼠收缩压(SBP)显著高于CIH1、对照组(P<0.05)和实验前水平(P<0.01).CIH2、CIH3组分别与CIH1和对照组比较:血管紧张素转化酶(ACE)及ACE2水平差异有统计学意义(P<0.05);血管紧张素(Ang)Ⅱ及血清丙二醛(MDA)、氧化低密度脂蛋白(ox-LDL)显著增高(P<0.05),Ang-(1-7)及血清抑制羟自由基能力则显著降低(P<0.05).SBP 与血清及肾Ang Ⅱ水平正相关;与Ang-(1-7)水平负相关;MDA、ox-LDL分别与血压及AngⅡ正相关,与Ang-(1-7)负相关;抑制羟自由基能力与血压、Ang Ⅱ负相关,与Ang-(1-7)正相关;oxLDL与MDA和抑制羟自由基能力分别呈正相关和负相关.CIH1组与对照组比较除SBP和血清AngⅡ(P<0.05)外其他指标差异无统计学意义(P>0.05),CIH2组与CIH3组以上指标差异均无统计学意义(P>0.05).结论 CIH 可引起大鼠氧化应激及RAS失衡,二者密切相关,可能是CIH诱导高血压发生的重要机制之一.NAC可能通过抗氧化作用调节RAS平衡而干预CIH相关性高血压的发生.

Abstract：

Objective To study the relation of oxidative stress with systolic blood pressure(SBP) and renin-agiotensin system(RAS) in a rat model of chronic intermitten hypoxia(CIH),and to investigate the preventive effect and mechanism of N-acetylcysteine (NAC) in CIH-induced hvpertension.Methods Twenty-four male Sprague-Dawley (SD) rats were divided into 4 groups:CIH + NAC group (CIH1),CIH +normal saline(NS) group(CIH2),CIH control group(CIH3)and blank control group(UC).CIH rats were subjected to alternating cycles of hypoxia (6%-8% O2 in N2 for 20-25 s) and normoxia (21% O2 in N2 for 2 min) every 180 s for 7 h per day.Rats in the CIH1 group were treated with NAC(800 ml · kg-1 · d-1)by intraperitoneal injection,and those in the CIH2 group were treated with NS (5 ml · kg-1 · d-1).Results SBP in the CIH2 and CIN3 groups at the end of 6th week was significantly elevated compared with the baseline SBP(P<.001)and those in the CIH1 and the UC groups (P<.05).The expression of angiotensinconverting enzyme(ACE) and ACE2 in renal arterioles was significantly different (P <0.05),and the levels of angiotensin Ⅱ(Ang Ⅱ)in the serum and kidney tissues,oxidation of low density lipoprotein (ox-LDL) and malondialdehyde (MDA)in the serum were increased.Ang-(1-7)and the inhibitory capability for hydroxyl free radicals in the serum were decreased significantly in CIH2 and CIH3 groups compared with CIH1 and UC (P <0.05)groups at the end of 6th week.SBP showed a positive correlation with Ang Ⅱ in serum and kidney tissues,but showed a negative correlation with Ang-(1-7)in serum and kidney tissues.The levels of MDS and ox-LDL in serum showed a positive correlation with Ang Ⅱ in serum and kidney tissues respectively,but showed a negative correlation with Ang-(1-7) in serum and kidney tissues respectively.The inhibitory capability for hydroxyl free radicals in serum showed a positive correlation with Ang-(1-7),but a negative correlation with Ang Ⅱ.The level of ox-LDL showed a positive correlation with MDA,but a negative correlation with the inhibitory capability for hydroxyl free radicals.There were no significant difference between CIH1 and UC groups in parameters except of SBP and Ang Ⅱ(P <0.05).All the data were not different between CIH2 and CIH3 groups(P>.05).Conclusions CIH caused oxidative stress and RAS imbalance in rats.The imbalance of RAS in CIH rats was related with oxidative stress.The imbalance of RAS and oxidative stress may be one of the important mechanisms for CIH-induced hypertension.NAC can prevent CIH-induced hypertension through modulation of RAS by its anti-oxidative effect.     

乙酰半胱氨酸镁对大鼠肝硬化门静脉高压的保护作用

目的 探讨乙酰半胱氨酸镁对大鼠肝硬化门静脉高压血管活性物质和肝纤维化指标的影响.方法 以12 μg· kg-1二甲基亚硝胺制备大鼠肝硬化模型,肝硬化造模完成后分组实验,乙酰半胱氨酸镁盐按25、50、100 mg·kg-1剂量每日分别腹腔注射进行肝硬化治疗,给药8周后处死大鼠取材进行各项指标测定.通过病理切片的检查、肝组织转化生长因子β1、一氧化氮、总一氧化氮合酶和诱导型一氧化氮合酶的检测来评价乙酰半胱氨酸镁盐治疗肝硬化门脉高压的效果.结果 二甲基亚硝胺造模结束后,模型组大鼠HE与网格染色结果显示其肝硬化处于Ⅲ-Ⅳ期;乙酰半胱氨酸镁低、中和高剂量组肝硬化程度明显轻于模型组,淋巴细胞浸润和假小叶形成减轻;治疗低、中和高剂量组转化生长因子β1指标明显低于模型组(P＜0.05);与模型组比较,各治疗组的一氧化氮、总一氧化氮合酶和诱导型一氧化氮合酶明显降低(P＜0.05).结论 乙酰半胱氨酸镁具有独特的抗氧化性,能清除体内各种自由基,调节配体依赖信号传导和细胞生长,对二甲基亚硝胺引起大鼠肝硬化门静脉高压症具有明显地保护作用.     

N-乙酰半胱氨酸对铜绿假单胞菌生物被膜影响的实验研究

目的研究N-乙酰半胱氨酸(NAC)单独作用对铜绿假单胞菌(PA)生物被膜(BF)形成的影响,以及与左氧氟沙星(LFX)合用对BF菌的清除作用。方法2005年6月至2006年6月在中南大学湘雅医院中心实验室中进行试验。扫描电镜(SEM)观察BF的形态,最小抑菌浓度(MIC)采用试管双倍稀释法测定;用甲基四氮唑蓝(MTT)比色法测定BF中活菌数。结果NAC能减少BF中基质样物质以及被膜的厚度,单用LFX需1MIC以上浓度才能使BF内活菌数明显下降。小剂量NAC(0.5g/L)与1/2MIC的LFX联合应用可使BF内活菌数明显下降,NAC对LFX的协同杀菌作用呈浓度依赖性。结论NAC能够抑制BF形成,并可增强LFX对PA生物被膜菌的杀菌活性。     

A knack for “NAC”: Treatment for heat stroke induced acute liver injury

IntroductionHeat stroke occurs when the body's core temperature becomes elevated above 40 °C, which may impact multiple organ systems. We present a case of heat stroke resulting in acute liver injury (ALI) successfully treated with intravenous N-acetylcysteine (NAC).Case presentationA 24-year-old unresponsive male without significant past medical history presented to the emergency department with heat stroke; his initial temperature was 107.4 °F. During his hospital course, he developed ALI with significant elevation in aspartate aminotransferase, alanine aminotransferase, and total bilirubin. These laboratory findings peaked by hospital day two, but improved prior to discharge on hospital day five and throughout his follow up clinic visits. His treatment course included cooling measures, supportive care, supplemental oxygen and airway management, seizure control, and intravenous NAC therapy.ConclusionHepatocellular injury is one of the most serious complications of heat stroke. We discuss the incidence and outcomes for patients who develop acute liver injury secondary to heat stroke and the use of NAC as an early potential therapeutic option.     

N-乙酰半胱氨酸对急性坏死性胰腺炎大鼠趋化因子MCP-1、MIP-2表达的影响

目的 探讨趋化因子单核细胞趋化蛋白1(MCP-1)与巨噬细胞炎性蛋白2(MIP-2)在大鼠急性坏死性胰腺炎(ANP)早期发病机制中的作用,并观察N-乙酰半胱氨酸(NAC)对趋化因子表达的影响.方法 35只SD大鼠随机分为假手术组(SO)组,ANP 3 h、6 h、12 h组和NAC干预3 h、6 h、12 h组,每组5只.采用4%牛磺胆酸钠胰胆管逆行注射制备ANP动物模型,NAC组在诱导ANP前0.5 h腹腔注射NAC 500 mg/kg.检测血淀粉酶、髓过氧化物酶(MPO),观察胰腺病理组织学改哪变,采用RT-PCR检测胰腺组织中MCP-1与MIP-2 mRNA的表达.结果 ANP各组血淀粉酶较高,浸润到胰腺组织的白细胞明显较多,胰腺病理损伤依次加重.SO组胰腺MCP-1 mRNA与MIP-2 mRNA表达阴性或弱表达(0.1492±0.0036、0.1593±0.0117),ANP各组MCP-1 mRNA(0.3653±0.0213、0.5890±0.0225、0.7164±0.0275)与MIP-2 mRNA(0.3871±0.0286、0.6040±0.0448、0.7692±0.0620)的表达随ANP病变的加重逐渐增强(均P＜0.01).MCP-1与MIP-2 mRNA的表达与胰腺的病理损伤成正相关r=0.76和0.82,P＜0.05).经NAC干预后,趋化因子MCP-1、MIP-2 mRNA表达下调(0.2497±0.0168、0.4457±0.0097、0.6306±0.0423,0.2436±0.0099、0.4312±0.0221、0.6302±0.0288,均 P＜0.05),白细胞浸润减少(0.63±0.03 vs 0.89±0.03,0.88±0.05 vs 1.42±0.14,1.31±0.09 vs 1.94±0.07,均P＜0.05),组织损伤得到改善(3.50±0.61 vs 5.10±0.42,5.60±0.65vs 7.50±0.50,7.50±0.79 vs 9.90±0.96,均P＜0.05).结论 ANP早期趋化因子MCP-1、MIP-2在胰腺组织中过表达,并参与白细胞的趋化作用.NAC能显著下调胰腺组织中趋化因子MCP-1、MIP-2的表达.     

Topical vitamin C,vitamin E,and acetylcysteine as corneal wound healing agents: A comparative study

Purpose:The purpose of this study was to evaluate wound healing abilities and efficacy of topical Vitamin C, Vitamin E, and acetylcysteine for their possible clinical use.Methods:The study was conducted on 36 eyes of 18 single-breed rabbits, Oryctolagus cuniculus, of both sexes. A 7.5 mm calibrated vacuum corneal trephine was used to induce a defect of 100 micron depth in center of both the corneas. The right eye of rabbits was selected as the control eye and the left eye as the trial eye, which received eyedrops as Group 1–10% Vitamin C eyedrops, Group 2–3% acetylcysteine eye drops, and Group 3–1% Vitamin E eye drops. Control eyes received ringer lactate. Evaluation was done for fluorescein stain positivity, epithelial defect size, and corneal haze on Day 2, Day 7, and Day 14 post induction of the epithelial defect.Results:On day 14, three eyes of control group, all Vitamin C and acetylcysteine treated eyes, and four Vitamin E treated eyes were fluorescein stain negative. The mean defect area on day 14 was 0, 0, 0.13, and 1.86 mm² in Vitamin C, Vitamin E, acetylcysteine, and control eyes, respectively. Vitamin C and Vitamin E control corneal haze better than acetylcysteine in experimentally induced corneal wounds in rabbits.Conclusion:The three trial drugs with different mechanism of action showed similar effect on healing of the experimentally created corneal wounds in rabbits, with comparison showing statistical insignificance.