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n-acetylcysteine ameliorates erectile dysfunction in rats with hyperlipidemia by inhibiting oxidative stress and corpus cavernosum smooth muscle cells phenotypic modulation

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Asian Journal of Andrology 2024年第1期26卷 99-106页

作者： Wei Ding Jun-Hong Fan Li-Ren Zhong nan-Xiong Wang Lu-Hao Liu Hai-Bo Zhang Li Wang Ming-Qiang Wang Bing-Lin He An-Yang Wei Department of Urology The First Affiliated Hospital of Guizhou University of Traditional Chinese MedicineGuiyang 550002China Department of Urology Guangdong Provincial People's HospitalGuangdong Academy of Medical SciencesGuangzhou 510000China Department of Urology Nanfang HospitalSouthern Medical UniversityGuangzhou 510000China Department of Urology Shenzhen Immigration Inspection General Station HospitalShenzhen 518000China Department of Organ Transplantation The Second Affiliated Hospital of Guangzhou Medical UniversityGuangzhou 510000China Department of Endocrinology The First Affiliated Hospital of Guizhou University of Traditional Chinese MedicineGuiyang 550002China

Hyperlipidemia is a major risk factor for erectile dysfunction(ED).Oxidative stress and phenotypic modulation of corpus cavernosum smooth muscle cells(CcSMCs)are the key pathological factors of ED.n-acetylcysteine(nAC)can inhibit oxidative stress;however,whether nAc can alleviate pathological variations in the corpus cavernosum and promote erectile function recovery in hyperlipidemic rats remains unclear.A hyperlipidemia model was established using 27 eight-week-old male Sprague-Dawley(SD)rats fed a high-fat and high-cholesterol diet(hyperlipidemic rats,HR).In addition,9 male SD rats were fed a normal diet to serve as controls(nC).HR rats were divided into three groups:HR,HR+normal saline(nS),and HR+nAC(n=9 for each group;nS or nAc intraperitoneal injections were administered daily for 16 weeks).Subsequently,the lipid profiles,erectile function,oxidative stress,phenotypic modulation markers of ccsMCs,and tissue histology were analyzed.The experimental results revealed that erectile function was significantly impaired in the HR and HR+nS groups,but enhanced in the HR+nAC group.Abnormal lipid levels,over-activated oxidative stress,and multi-organ lesions observed in the HR and HR+nS groups were improved in the HR+nAC group.Moreover,the HR group showed significant phenotypic modulation of CCSMCs,which was also inhibited by nAC treatment.This report focuses on the therapeutic effect of nAc in restoring erectile function using a hyperlipidemic rat model by preventing CcSMC phenotypic modulationand attenuating oxidativestress.

关键词： erectile dysfunction hyperlipidemia n-acetylcysteine oxidative stress henotypic modulation

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Ferroptosis inhibitors reduce celastrol toxicity and preserve its insulin sensitizing effects in insulin resistant HepG2 cells

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Journal of Integrative Medicine 2024年第3期22卷 286-294页

作者： Jia-jia Liu Xue Zhang Bang-lan Cai Man-man Qi Yong-bin Chi Bin Peng Deng-hai Zhang School of Medicine Shanghai UniversityShanghai 200444China Shanghai Health Commission Key Lab of Artificial Intelligence-Based Management of Inflammation and Chronic Diseases Shanghai Pudong Gongli HospitalSecondary Military Medical UniversityShanghai 200135China School of Basic Medicine Ningxia Medical UniversityYinchuan 750004Ningxia Hui Autonomous RegionChina

Objective:Research has shown that celastrol can effectively treat a variety of diseases,yet when passing a certain dosage threshold,celastrol becomes toxic,causing complications such as liver and kidney damage and erythrocytopenia,among others.With this dichotomy in mind,it is extremely important to find ways to preserve celastrol’s efficacy while reducing or preventing its toxicity.Methods:In this study,insulin-resistant Hep G2(IR-Hep G2)cells were prepared using palmitic acid and used for in vitro experiments.IR-Hep G2 cells were treated with celastrol alone or in combination with nacetylcysteine(nAC)or ferrostatin-1(Fer-1)for 12,24 or 48 h,at a range of doses.Cell counting kit-8assay,Western blotting,quantitative reverse transcription-polymerase chain reaction,glucose consumption assessment,and flow cytometry were performed to measure celastrol’s cytotoxicity and whether the cell death was linked to ferroptosis.Results:Celastrol treatment increased lipid oxidation and decreased expression of anti-ferroptosis proteins in IR-Hep G2 cells.Celastrol downregulated glutathione peroxidase 4(GPX4)m RnA.Molecular docking models predicted that solute carrier family 7 member 11(SLC7A11)and GPX4 were covalently bound by celastrol.Importantly,we found for the first time that the application of ferroptosis inhibitors(especially nAC)was able to reduce celastrol’s toxicity while preserving its ability to improve insulin sensitivity in IR-Hep G2 cells.Conclusion:One potential mechanism of celastrol’s cytotoxicity is the induction of ferroptosis,which can be alleviated by treatment with ferroptosis inhibitors.These findings provide a new strategy to block celastrol’s toxicity while preserving its therapeutic effects.

关键词： Celastrol Insulin resistance Ferroptosis n-acetylcysteine Palmitic acid Molecular docking

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Evaluation of n-acetylcysteine and glutathione as quenching agents for the analysis of halogenated disinfection by-products

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Journal of Environmental Sciences 2022年第7期34卷 71-79页

作者： Shunke Ding Menglin Wu Rong Xiao Chao Fang Qi Wang Bin Xu Wenhai Chu State Key Laboratory of Pollution Control and Resource Reuse College of Environmental Science and EngineeringTongji UniversityShanghai 200092China Key Laboratory of Yangtze River Water Environment Ministry of EducationTongji UniversityShanghai 200092China School of Life and Environmental Science Wenzhou UniversityZhejiang 325035China

Disinfection by-products(DBPs), formed from the reactions of disinfectants with natural organic matter and halides in drinking water, were considered to be cytotoxic and genotoxic, and might trigger various cancers. The relatively low concentration of DBPs in finished water(low μg/L or even ng/L levels) and the interference from water matrix inhibited in situ determination of DBPs. Moreover, the further formation and degradation of DBPs by disinfectants during the holding time(several hours to several days) from sample collection to analysis could adversely affect the determination of DBPs. To obtain accurate, precise and reliable data of DBP occurrence and formation, robust and reliable sample preservation is indispensable. However, the commonly used quenching agents(e.g., sodium sulfite, sodium thiosulfate, and ascorbic acid) for sample preservation can decompose reactive DBPs by reductive dehalogenation. This study evaluated the performance of n-acetylcysteine(nAC) and glutathione(GSH) as quenching agents for the analysis of halogenated DBPs by investigating the stoichiometry of the disinfectant-quenching agent reaction, the formation of DBPs during chlor(am)ination of nAC or GSH, and the effects of nAC or GSH on the stability of 18 individual DBPs and total organic halogen(TOX). Based on the results of this study, nAC and GSH were considered to be ideal quenching agents for the analysis of most DBPs and TOX, except halonitromethanes.

关键词： Disinfection by-products Total organic halogen Quenching agents n-acetylcysteine Glutathione

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Effects of n-acetylcysteine on growth,viability and reactive oxygen species levels in small antral follicles cultured in vitro

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Asian pacific Journal of Reproduction 2023年第1期12卷 42-48页

作者： Efigênia B.Cordeiro Bianca R.Silva Laís R.F.M.Paulino Pedro A.A.Barroso Laryssa G.Barrozo Miguel F.de Lima neto JoséR.V.Silva Laboratory of Biotechnology and Physiology of Reproduction Federal University of CearaAv.Comandante Maurocélio Rocha Ponte 10062041-040SobralCEBrazil

Objective:To investigate the effects of different concentrations of n-acetylcysteine on follicular growth and morphology,as well as on viability,levels of reactive oxygen species(ROS)and meiotic progression of oocytes from in vitro cultured bovine early antral follicles.Methods:Isolated early antral follicles(about 500μm)were cultured in TCM-199+alone or supplemented with 1.0,5.0 or 25.0 mM n-acetylcysteine at 38.5℃with 5%CO_(2) for 8 days.Follicle diameters were evaluated at day 0,4 and 8 of culture.At the end of culture,the levels of ROS,chromatin configuration and viability(calcein-AM and ethidium homodimer-1 staining)were investigated in the cumulus-oocyte complexes.Comparisons of follicle diameters between treatments were performed.Data on percentages of morphologically normal follicles,growth rates and chromatin configuration in different treatments were compared.Results:An increase in follicular diameters after culture in all treatments was observed,except for follicles cultured with 25.0 mM n-acetylcysteine.Fluorescence microscopy showed that oocytes cultured in all treatments were stained positively with calcein AM,and that 5.0 mM n-acetylcysteine reduced fluorescence for ethidium homodimer-1.Intracellular levels of ROS in oocytes from follicles cultured with 1.0 mM n-acetylcysteine showed a significant reduction compared to other treatments.The presence of n-acetylcysteine in culture medium did not influence the rates of oocyte at the germinal vesicle stage.Conclusions:n-acetylcysteine at concentrations of 1.0 and 5.0 mM reduces ROS levels and staining for ethidium homodimer-1 in in vitro cultured follicles,respectively,while 25.0 mM n-acetylcysteine decreases follicular growth and the percentages of continuously growing follicles.

关键词： Antioxidant n-acetylcysteine Antral follicles Bovine Reactive oxygen species

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Effects of n-acetylcysteine on Clara cells in rats with cigarette smoke exposure

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Chinese Medical Journal 2010年第4期123卷 412-417页

作者： LIAO Ji-ping CHI Chun-hua LI Hai-chao TAnG Xiu-ying Department of Respiratory Medicine Peking University First Hospital Beijing 100034 China Department of Pathology Peking University First Hospital Beijing 100034 China

Background The number of Clara cells and the Clara cell 16-kDa protein （CC16） levels of the lung decrease in patients with chronic obstructive pulmonary disease （COPD）. n-acetylcysteine （nAC） is a powerful antioxidant and can reduce the frequency of acute exacerbations of COPD. But the exact mechanism is unclear. The present study was designed to investigate the effects of nAC on Clara cells in rats with cigarette smoke exposure. Methods Eighteen adult male Wistar rats were randomly divided into 3 groups, 12 exposed to cigarette smoke （CS） thrice a day, 10 cigarettes for 30 minutes each time for 1 week, without （CS group） or with （CS＋nAC group） oral intake of nAC 80 mg·kg^-1·d^-1, and another 6 rats exposed to fresh air （control group）. Clara cells were observed by an electron microscope. The mRnA expression of CC16 and CC16 protein in lungs were determined by reverse transcription polymerase chain reaction （RT-PCR） and immunohistochemistry respectively. The glutathion （GSH） level in plasma and lung tissue were tested by fluorimetry assay. Results Compared with the controls, the pathologic score of small airways significantly increased in the CS exposed rats （20.3±14.7 vs. 53.7±11.5, P 〈0.05）. The Clara cell particles in cytoplasm decreased in the CS group （P 〈0.05）. The percentage of CC16-positive cells in bronchioles in the CS group （27.8±4.3 and 29.5±2.4 in terminal bronchioles and respiratory bronchioles, respectively） significantly decreased as compared with the control group （37.1±3.8 and 43.8±5.8 in terminal bronchioles and respiratory bronchioles, respectively）（P 〈0.05）. no significant difference was observed in GSH level （（181±26） nmol/L in the control group vs. （170±18） nmol/L in the CS group） between the two groups. After treatment with nAC, the pathologic score of small airways （24.1±17.5） decreased （P 〈0.05）. Clara cell particles in cytoplasm of Clara cells increased and GSH level in plasma （（213±40） nmol/L vs. （170±18） nmol/L in the CS group） increased too （P 〈0.05）, while the increase in the propo

关键词： tobacco smoke pollution Clara cells n-acetylcysteine glutathion

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Protective Effect of Salidroside on Contrast-Induced nephropathy in Comparison with n-acetylcysteine and Its Underlying Mechanism

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Chinese Journal of Integrative Medicine 2015年第4期21卷 266-273页

作者：邢悦魏日胞唐露杨悦郑晓勇王子承高玉伟 State Discipline and State Key Laboratory of Kidney Disease (Chinese PLA General Hospital 2011 DAV00088) Department of Rheumatism Immunity Tianjin First Center Hospital

Objective： TO study the prevention effect of salidroside on contrast-induced-nephropathy （CIn） and its underlying mechanism. Methods： A total of 24 Wistar rats were randomly divided into 4 groups with 6 in each group. Rats were firstly administrated with normal saline （control and model groups）, n-acetylcysteine （nAC, nAC group） and salidroside （salidroside group） for 7 days before model establishment in each group, respectively. Histopathological analysis was performed by periodic acid-Schiff （PAS） staining. Oxidative stress related parameters including superoxide dismutase （SOD） and methane dicarboxylic aldehyde （MDA）, nitric oxide （nO）, angiotensin 11 （Ang II）, 8-hydroxy-2＇-deoxyguanosine （8-OHdG）, mRnA and protein levels of endothelial nitric oxide synthase （enOS）, and nitric oxide synthase （nOS） activity were measured. Results： Compared with the control group, the levels of MDA, Ang II and 8-OHdG were all significantly increased and levels of SOD, nO, and enOS mRnA and protein were decreased significantly in the model group （P〈0.05）. Meanwhile, the nOS activity was also significantly decreased in the model group （P〈0.05）. In addition, the levels of these parameters were all improved in the nAC （P〈0.05） and salidroside groups and no significant different was found between these two groups （P〉0.05）. Conclusion： Salidroside can be the potential substitute Of nAC to prevent CIn. The underlying mechanism may be associated with oxidative stress damage caused by contrast agents.

关键词： salidroside contrast-induced-nephropathy oxidative stress n-acetylcysteine Chinese medicine

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n-acetylcysteine maintains penile length and erectile function in bilateral cavernous nerve crush rat model by reducing penile fibrosis

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Asian Journal of Andrology 2021年第2期23卷 215-221页

作者： Ming Ma Chang-Jing Wu Peng Zhang Tao Li Shan-Zun Wei Bo-Tao Yu Feng Qin Jiu-Hong Yuan Andrology Laboratory West China HospitalSichuan UniversityChengdu 610041China Department of Urology West China HospitalSichuan UniversityChengdu 610041China

Penile length shortening and erectile dysfunction are common complications after radical prostatectomy.Various methods have been used to maintain erectile function,but less attention has been paid to preserving penis length.n-acetylcysteine(nAC)has the effect of antioxidation and antifibrotic,which may be beneficial to improve those postoperative complications.This study investigated the effect of nAC on maintaining the penile length and the erectile function after bilateral cavernous nerve crush(BCnC)and its underlying mechanism.Twenty-four male rats were randomly divided into three groups:control group,BCnC group,and BCnC+nAC group.nAC or equal volume of saline was daily administrated by intragastric gavage for 4 weeks.The initial and end penile lengths were measured.Intracavernosal pressure/mean arterial pressure(ICP/MAP)ratio was calculated to assess erectile function.Hematoxylin-eosin staining,Masson's trichrome staining,immunohistochemistry,and Western blot were performed to explore cellular and molecular changes of the penis.Compared to the BCnC group,the penile length,ICP/MAP ratio and smooth muscle/collagen ratio in the BCnC+nAC group were improved significantly(all Pnd the expressions of endothelial nitric oxide synthase,α-smooth muscle actin,glutathione,and glutathione peroxidase 1 were significantly increased after nAC treated(all Png with the decreased expressions of hypoxia-inducible factor-1α,transforming growth factor-β1,collagen I,collagen III,collagen IV,malonaldehyde,and lysine oxidase(all Pnstrated that nAC could maintain penile length and partly improve erectile function.Possible mechanism is directly and/or indirectly related to antihypoxic and antifibrosis.

关键词： erectile dysfunction n-acetylcysteine penile fibrosis penile length

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Pathogenesis of cigarette smoke-induced chronic obstructive pulmonary disease and therapeutic effects of glucocorticoids and n-acetylcysteine in rats

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Chinese Medical Journal 2004年第11期117卷 1611-1619页

作者：徐凌蔡柏蔷朱元珏 Department of Respiratory Medicine Peking Union Medical College Hospital Peking Union Medical College Chinese Academy of Medical Sciences Beijing 100730 China

Background T lymphocytes and matrix metalloproteinase (MMP) play an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD). However, the details of the mechanisms involved are unclear. The aims of this study were to investigate the changes in interferon-γ (IFn-γ), interleukin-4 (IL-4), MMP-9, MMP-12 and tissue inhibitor of metalloproteinase-1 (TIMP-1) levels in a smoke-induced COPD rat model and the therapeutic effects of glucocorticoids and n-acetylcysteine.Methods Male Wistar rats were exposed to cigarette smoke for 3.5 months. Budesonide or n-acetylcysteine was given in the last month. Lung function was measured at the end of the study. IL-4 and IFn-γ levels were then determined in bronchoalveolar lavage fluid and lung tissue samples by enzyme -linked immunosorbent assay. The expression of MMP-9, MMP-12 and TIMP-1 mRnA in lung tissue was determined by RT-PCR. Results In comparison with the control group, rats exposed to smoke had a significant increase in IL-4 and MMP-12 levels and a significa nt decrease in IFn-γ levels. In addition, the IL-4/ IFn-γ ratio and MMP-12/TIMP-1 ratio were both higher. At the same time, the ratio of forced expiratory volume in 0.3 second to forced vital capacity (FEV 0.3/FVC) and dynamic compliance (C dyn) decreased and expiratory resistance (Re) increased. By measuring pulmonary mean linear intercept and mean alveolar numbers, obvious emphysematous changes were observed in the smoke exposed group. After treatment with budesonide, IL-4 and MMP-12 decreased and IFn-γ increased. The IL-4/IFn-γ ratio returned to normal, though the MMP-12/TIMP-1 ratio remained unchanged. FEV 0.3/FVC was significantly higher and Re was significantly lower than that in untreated smoke exposed rats. no significant differences were found in pulmonary mean linear intercept and mean alveolar numbers. After treatment with n-acetylcysteine, IFn-γ increased and the IL-4/IFn-γ ratio decreased. The MMP-12/TIMP-1 ratio remained unchanged. Re and C dyn both improved obv

关键词： pulmonary disease chronic obstructive cytokine s· glucocorticiods n-acetylcysteine

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n-acetylcysteine and reduced glutathione reverse flupirtine-induced liver injury and pro⁃duce other beneficial effects in combination with flupirtine

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中国药理学与毒理学杂志 2023年第S1期37卷 28-29页

作者： CHEn Yanming CHEn Jinsong Peking University Health Science Center Beijing 100000China Xuzhou Food and Drug Supervision and Inspection Center Xuzhou221000China

OBJECTIVE To assess whether n-acetylcysteine(nAC)and reduced glutathione(GSH)are effective in reversing flupirtine-induced hepatotoxicity and whether they have other beneficial effects when combined with flupirtine.METHODS The analgesic effects of nAC and flupirtine were first evaluated in carrageenaninduced inflammatory pain and paclitaxel-induced neuropathic pain.The combination subthreshold⁃ing approach was then used to determine whether the combination of nAC and flupirtine produced synergistic analgesic effects.Hepatotoxicity markers and histopathological examination of the liver were used to assess the efficacy of nAC and GSH in reversing flupirtine-induced hepato⁃toxicity.Finally,the effect of GSH on the safe range of flupirtine was assessed in an acute tox⁃icity assay.RESULTS Flupirtine and nAC pro⁃duced dose-dependent antiallodynic effects evoked by carrageenan and paclitaxel in mice.In the above model,the combination of nAC and flupirtine produced an unexpected synergistic analgesic effect.There were no significant differ⁃ences observed in the hepatotoxicity markers and liver histopathology between the experimen⁃tal group and the control group under nAC and GSH treatment.Finally,GSH(200 mg·kg^(-1))expanded the therapeutic index of flupirtine by 1.77 times.COnCLUSIOn nAC and GSH are effective in preventing liver damage caused by long-term flupirtine use,which provides a solu⁃tion for the safe and effective treatment of chronic pain with flupirtine.In addition,the other benefi⁃cial effects of nAC and GSH when combined with flupirtine may provide the basis for the devel⁃opment of a new therapy with minimal sideeffects and good efficacy.

关键词： n-acetylcysteine reduced glutathione flupirtine hepatotoxicity

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n-acetylcysteine attenuates lipopolysaccharide-induced apoptotic liver damage in D-galactosamine-sensitized mice

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Acta Pharmacologica Sinica 2007年第11期28卷 1803-1809页

作者： Hua WAnG~2,De-xiang XU~(2,3,4),Jin-wei LU~2,Lei ZHAO~2,Cheng ZHAnG~2,Wei WEI~(3,4)~2 Department of Toxieology and ~2 Institute of Clinical Pharmacology Anhui Medical University,Hefei 230032,China Department of Toxicology Anhui Medical University Hefei China Institute of Clinical Pharmacology Anhui Medical University Hefei China

Aim:To investigate the effects of n-acetylcysteine on D-galactosamine (Ga1n)/lipopolysaccharide (LPS)-induced apoptotic liver injury in mice.Methods:Whengiven together with a low dose of LPS,Ga1n highly sensitizes animals to produceapoptotic liver injury with severe hepatic congestion,resulting in rapid death.Inthe Ga1n/LPS model,TnF-α is the major mediator leading to apoptotic liver injury.Reactive oxygen species (ROS) are involved in Ga1n-induced sensitization toTnF-α-evoked hepatocyte apoptosis.n-acetylcysteine (nAC) is an antioxidantand a glutathione (GSH) precursor.In this study,we investigated the effects ofnAC on LPS-induced apoptotic liver injury in Ga1n-sensitized mice.Results:Pretreatment with nAC significantly reduced Ga1n/LPS-induced elevation ofserum alanine aminotransferase levels.In parallel,Ga1n/LPS-induced hepaticnecrosis and congestion were obviously improved by nAC.Furthermore,nACpretreatment significantly alleviated Ga1n/LPS-induced hepatic apoptosis,mea-sured by the inhibition of hepatic caspase-3 activity and attenuation of DnAladdering.nAC pretreatment had no effect on LPS-evoked nitric oxide productionin Ga1n-sensitized mice.Increases in serum TnF-α concentration,which wereobserved in Ga1n/LPS-treated mice,were not significantly reduced by nAC.Although nAC pretreatment significantly alleviated LPS-induced hepatic GSHdepletion,DL-buthionine-(SR)-sulfoximine,an inhibitor of GSH synthesis,did notinfluence the protective effect of nAC on Ga1n/LPS-induced apoptotic liver injury.Conclusion:nAC attenuates Ga1n/LPS-induced apoptotic liver injury via its strongROS scavenging and anti-apoptotic effects.

关键词： n-acetylcysteine lipopolysaccharide apoptosis liver injury antioxidant

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