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pyrrolidine dithiocarbamate alleviates the anti-tuberculosis drug-induced liver injury through JAK2/STAT3 signaling pathway:An experimental study

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Asian Pacific Journal of Tropical Medicine 2017年第5期10卷 493-496页

作者： Hong Zhang Yang Liu Li-Kun Wang Na Wei Internal Medicine Department No.2 Linyi Chest Hospital in Shandong ProvinceLinyi CityShandong Province 276034China Child Healthcare Department Linyi Chest Hospital in Shandong ProvinceLinyi CityShandong Province 276034China Infectious Disease Department No.6 Ward Linyi People's Hospital in Shandong ProvinceLinyi CityShandong Province 276034China Laboratory Department Linyi Chest Hospital in Shandong ProvinceLinyi CityShandong Province 276034China

Objective:To study the effect of pyrrolidine dithiocarbamate(PDTC) on the anti-tuberculosis drug-induced liver injury and the molecular mechanism. Methods:Clean male SD rats were selected as experimental animals and randomly divided into normal group,model group,PDTC group and AG490 group. Animal model of anti-tuberculosis drug-induced liver injury was established by intragastric administration isoniazid + rifampicin. PDTC group received intraperitoneal injection of PDTC,and AG490 group received intraperitoneal injection of AG490. Twenty-eight days after intervention,the rats were executed,and the liver injury indexes,inflammation indexes and oxidative stress indexes in serum as well as JAK2/STAT3 expression,liver injury indexes,inflammation indexes and oxidative stress indexes in liver tissue were determined. Results:p-JAK2,p-STAT3,TNF-α,IL-1β,IL-6,ROS,8-OHdG and MDA expression in liver tissue as well as TBIL,ALT,AST,γ-GT,TNF-α,IL-1β,IL-6,ROS,8-OHdG and MDA levels in serum of model group were significantly higher than those of normal group while p-JAK2,p-STAT3,TNF-α,IL-1β,IL-6,ROS,8-OHdG and MDA expression in liver tissu as well as TBIL,ALT,AST,γ-GT,TNF-α,IL-1β,IL-6,ROS,8-OHdG and MDA levels in serum of PDTC group and AG490 group were significantly lower than those of model group. Conclusions:PDTC can inhibit the inflammation and oxidative stress mediated by JAK2/STAT3 signaling pathway to alleviate the anti-tuberculosis drug-induced liver injury.

关键词： Drug-induced liver injury Anti-tuberculosis drug pyrrolidine dithiocarbamate JAK2 STAT3

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Protective effect of pyrrolidine dithiocarbamate on liver injury induced by intestinal ischemia-reperfusion in rats

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Hepatobiliary & Pancreatic Diseases International 2006年第1期5卷 90-95页

作者： Xiao-Feng Tian, Ji-Hong Yao, Ying-Hua Li, Hai-Feng Gao, Zhen-Zhen Wang, Chun-Ming Yang and Shu-Sen Zheng Department of General Surgery, Second Affiliated Hospital of Dalian Medical University, Dalian 116027, China Department of Pharmacology, Dalian Medical University, Dalian 116027, China and Department of Hepatobiliary and Pancreatic Surgery, First Affiliated Hospital, Zhejiang University School of Medicine. Hangzhou 310003, China Department of General Surgery Second Affiliated Hospital of Dalian Medical University Dalian 116027 China. txfdl@***

BACKGROUND: The nuclear translocation of transcription factors may be a critical factor in the intracellular pathway involved in ischemia/reperfusion(I/R) injury. The aim of the study was to evaluate the role of nuclear factor-kappa B (NF-κB) in the pathogenesis of liver injury induced by intestinal ischemia/reperfusion (IIR) and to investigate the effect of pyrrolidine dithiocarbamate (PDTC) on this liver injury. METHODS: Male Wistar rats were divided randomly into three experimental groups (8 rats in each): sham operation group (control group); intestinal/reperfusion group(I/R group): animals received 1-hour of intestinal ischemia and 2-hour reperfusion; and PDTC treatment group (PDTC group): animals that received I/R subject to PDTC treatment (100 mg/kg). The histological changes in the liver and intestine were observed, and the serum levels of tumor necrosis factor-α (TNF-α), alanine aminotransferase (ALT), aspartate aminotransferase (AST), liver superoxide dismutase (SOD), and nitrite/nitrate (NO) were measured. The immunohistochemical expression and Western blot analysis of liver NF-κB and intercellular adhesion molecule-1(ICAM-1) were observed. RESULTS: IIR induced liver injury characterized by the histological changes of liver edema, hemorrhage, polymorphonuclear neutrophil (PMN) infiltration, and elevated serum levels of AST and ALT. The serum TNF-α level was significantly higher than that of the control group(P<0.01) and a high level of liver oxidant product was observed (P<0.01). These changes were parallel to the positive expression of NF-κB and ICAM-1. After the administration of PDTC, the histological changes after liver injury were improved; the levels of SOD and NO in the liver were elevated and reduced, respectively (P<0.01). The expressions of ICAM-1 and NF-κB in the liver were weakened (P<0.01). CONCLUSION: NF-κB plays an important role in the pathogenesis of liver injury induced by HR. PDTC, an agent known to inhibit the activation of NF-κB, can

关键词： liver injury intestinal ischemia/reperfusion nuclear factor kappa B pyrrolidine dithiocarbamate

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Activation of nuclear factor-kappa B and effects of pyrrolidine dithiocarbamate on TNBS-induced rat colitis

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World Journal of Gastroenterology 2005年第10期11卷 1508-1514页

作者： KenChen You-MingLong HuiWang LeiLan Zhen-HeLin DepartmentofClinicalMedicine GuangdongCollegeofPharmacyGuangzhou510224GuangdongProvinceChina DepartmentofPharmacology GuangdongMedicalCollegeZhanjiang524023GuangdongProvinceChina DepartmentofDigestion theAffiliatedHospitalofGuangdongMedicalCollegeZhanjiang524023GuangdongProvinceChina

AIM: To explore the changes of nuclear factor-kappa B (NF-κB) DNA-binding activity, the expression of intercellular adhesion molecule-1(ICAM-1) regulated by IMF-κB at various times and to evaluate the effects of pyrrolidine dithiocarbamate (PDTC) on trinitrobenzene sulfonic acid (TNBS)-induced rat colitis. METHODS: TNBS of 0.6 mL was mixed with ethanol of 0.3 mL solution and instilled into the lumen of the rat colon. The rat models were divided into 6 groups, which were killed at 24 h, 3, 7,14, and 21 d after enema. Colonic inflammation and damage were assessed by macroscopical and histological criteria. Activity of NF-κB DNA-binding was analyzed by electrophoresis mobility shift assays (EMSA). Expression of ICAM-1 was detected by in situ hybridization (ISH) and immunohistochemistry (IH). Then various doses of PDTC were injected into rat abdomen 30 min before enema with TNBS/ethanol as pretreatment. The rats were killed 4 h after enema and the colonic inflammation, myeloperoxidase (MPO) activity, malondialdehyde (MDA) level, and DNA-binding activity of NF-κB were assessed. Finally, PDTC was injected intraperitoneally after colitis was induced. Changes of morphology were assayed. RESULTS: During the first week, hyperemia, hemorrhage, edema and ulceration of the colonic mucosa appeared with predominant infiltration of leukocytes. Neutrophils, macrophages, lymphocytes infiltrated in mucosa and submucosa 14 d later. Fibroblasts and granuloma-like structures were also obviously seen. The binding activity of NF-κB began to increase at 24 h time point and reached a peak at 14 d, then decreased but still was higher than control group at 21 d (P<0.01). Levels of ICAM-1 mRNA and protein significantly elevated at 24 h and the peak was at 21 d. Pretreatment with PDTC could attenuate the development of inflammation but not by reducing NF-KB activity. This attenuation of inflammation had a positive relationship with the dose of PDTC. PDTC at the dose of 100 mg/kg had no therapeut

关键词： Nuclear factor pyrrolidine dithiocarbamate Rat Colitis

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Evaluation of the effect of pyrrolidine dithiocarbamate in suppressing inflammation in mice with dextran sodium sulfate-induced colitis

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World Journal of Gastroenterology 2007年第11期13卷 1666-1671页

作者： Ichiro Hirata Shingo Yasumoto Ken Toshina Takuya Inoue Takashi Nishikawa Naoko Murano Mitsuyuki Murano Fang-Yu Wang Ken-ichi Katsu Department of Gastroenterology Fujita Health University Jaoan Second Department of Internal Medicine Osaka Medical College Japan Department of Gastroenterology Jinling Hospital Nanjing University School of Medicine Nanjing 210002 Jiangsu Province China

AIM: To evaluate the effect of pyrrolidine dithio- carbamate (PDTC; an NF-κB inhibitor) administered at low (50 mg/kg) and high (100 mg/kg) doses in suppressing colitis in mice with dextran sodium sulfate (DSS)-induced colitis. METHODS: Mice were divided into a DSS-untreated group (normal group), DSS-treated control group, DSS+PDTC-treated groupⅠ(low-dose group), and DSS+PDTC-treated groupⅡ (high-dose group). In each group, the disease activity index score (DAI score), intestinal length, histological score, and the levels of activated NF-κB and inflammatory cytokines (IL-1β and TNF-α) in tissue were measured. RESULTS: The DSS+PDTC-treated groupⅡ exhibited suppression of shortening of intestinal length and reduction of DAI score. Activated NF-κB level and IL-1β and TNF-α levels were significantly lower in DSS+PDTC- treated groupⅡ. CONCLUSION: These findings suggest that PDTC is useful for the treatment of ulcerative colitis.

关键词： Ulcerative colitis DSS-induced colitis pyrrolidine dithiocarbamate NF-κB Mice

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S-adenosyl-L-methionine modifies antioxidant-enzymes,glutathione-biosynthesis and methionine adenosyltransferases-1/2 in hepatitis C virus-expressing cells

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World Journal of Gastroenterology 2016年第14期22卷 3746-3757页

作者： Sonia Amelia Lozano-Sepulveda Eduardo Bautista-Osorio Jose Angel Merino-Mascorro Marta Varela-Rey Linda Elsa Munoz-Espinosa Paula Cordero-Perez María Luz Martinez-Chantar Ana Maria Rivas-Estilla Department of Biochemistry and Molecular Medicine School of Medicine Autonomous University of Nuevo Leon Monterrey Metabolomic Unit CIC bio GUNE CIBERehd Parque Tecnológico de Bizkaia Liver Unit School of Medicine and Hospital Universitario Autonomous University of Nuevo Leon

AIM: To elucidate the mechanism(s) by which S-adenosyl-L-methionine(SAM) decreases hepatitis C virus(HCV) ***: We examined the effects of SAM on viral expression using an HCV subgenomic replicon cell culture system. Huh7 HCV-replicon cells were treated with 1 mmol/L SAM for different times(24-72 h), then total RNA and proteins were isolated. c DNA was synthesized and real time-PCR was achieved to quantify HCV-RNA, superoxide dismutase 1 and 2(SOD-1, SOD-2) catalase, thioredoxin 1, methionine adenosyltransferase 1A and 2A(MAT1A, MAT2A) expression, and GAPDH and RPS18 as endogenous genes. Expression of cellular and viral protein was evaluated by western-blot analysis using antibodies vs HCV-NS5 A, SOD-1, SOD-2, catalase, thioredoxin-1, MAT1 A, MAT2 A, GAPDH and actin. Total glutathione levels were measured at different times by Ellman's recycling method(0-24 h). Reactive oxidative species(ROS) levels were quantified by the dichlorofluorescein assay(0-48 h); Pyrrolidin dithiocarbamate(PDTC) was tested as an antioxidant control and H2O2 as a positive oxidant ***: SAM exposition decreased HCV-RNA levels 50%-70% compared to non-treated controls(24-72 h). SAM induced a synergic antiviral effect with standard IFN treatment but it was independent of IFN signaling. In addition, 1 mmol/L SAM exposition did not modify viral RNA stability, but it needs cellular translation machinery in order to decrease HCV expression. Total glutathione levels increased upon SAM treatment in HCV-replicon cells. Transcriptional antioxidant enzyme expression(SOD-1, SOD-2 and thioredoxin-1) was increased at different times but interestingly, there was no significant change in ROS levels upon SAM treatment, contrary to what was detected with PDTC treatment, where an average 40% reduction was observed in exposed cells. There was a turnover from MAT1A/MAT2 A, since MAT1 A expression was increased(2.5 fold-times at 48 h) and MAT2 A was diminished(from 24 h) upon SAM treatment a

关键词： Hepatitis C virus S-adenosyl-L-methionine Superoxide dismutase 1 Superoxide dismutase 2 Replication Hepatitis C virus-RNA NS5A Oxidative stress Antioxidants Viral proteins Reactive oxygen species pyrrolidine dithiocarbamate

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The Effects of PDTC on Interleukin-1β-induced Nitric Oxide Production in Chondrocytes

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2009年第3期29卷 300-303页

作者：刘建湘杜靖远杨述华邱晓华刘日光易诚青李新春 Department of Orthopedics Union Hospital Tongji Medical College Huazhong University of Science and Technology Department of Orthopedics the Affiliated Hospital of Guiyang Medical College Department of Orthopedics Shanghai First Hospital Department of Orthopedics Ningbo First Hospital

In order to find new drugs to inhibit nitric oxide （NO） production, the effects of pyrrolidine dithiocarbamate （PDTC）, a nuclear factor-kappa B （NF-κB） inhibitor, on recombinant human interleukin-1β （rhIL-1β）-induced NO production in chondrocytes were investigated. Rat chondrocytes were isolated and cultured, divided into control, P0, P1, P2, P3 and P4 groups. The chondrocytes in the P0, P1, P2, P3 and P4 groups were treated with different concentrations of PDTC （0, 3, 10, 30, and 50 ***/L respectively） for 1 h and then incubated with 5 U/mL rhIL-1β for 24 h. NO assay kit and RT-PCR were used to detect the NO content and the iNOS mRNA expression in the chondrocytes The expression level of iNOS mRNA in control, P0, P1, P2, P3 and P4 groups was 0.02±0.01, 1.24±0.13, 1.21±0.14, 0.61±0.11, 0.40±0.09, 0.21±0.06, and the relative content of NO was 15.8±2.7, 100±14.8, 92.6±9.3, 68.3±14.2, 27.5±9.8, 19.8±3.6, respectively. In the P0, P1, P2, P3 and P4 groups, the expression of iNOS mRNA and NO production were significantly increased as compared with those in the control group. As compared with the P0 group, the expression of iNOS mRNA and NO content in control group were lower. In the P2, P3 and P4 groups, PDTC could significantly inhibit the expression of iNOS and NO production induced by rhIL-1β in a concentration-dependent manner. It is suggested that PDTC can inhibit NO production and iNOS mRNA expression induced by IL-1β, which may provide an alternative method for the treatment of osteoarthritis.

关键词： pyrrolidine dithiocarbamate chondrocyte nitric oxide nuclear factor-kappa B

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Effects of PDTC on the Proliferation and PCNA Expression of Human Retinal Pigment Epithelial Cells

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2006年第2期26卷 238-240页

作者：胡军李贵刚 Department of Ophthalmology Tongji HospitalTongji Medical College Huazhong University of Science and Technology.Wuhan 430022China

To investigate the effects of pyrrolidine dithiocarbamate （PDTC） on the proliferation and PCNA （proliferating cell nuclear antigen） expression of cultured human retinal pigment epithelium cells, human retinal pigment epithelium cells （RPE） were cultured from normal adults who died accidentally. The effects of PDTC on the proliferation of RPE cells were examined by using methyl thiazlyl tetrazolium （MTT） assay. The effects of PDTC on the PCNA expression of RPE cells were immunohistochemically examined by employing biological image analysis system （BIAS）. After treatment with PDTC of various of concentration ranging from 0.062 to 1 g/L for 24 h, or concentrations ranging from 0.031 to 1 g/L, the proliferation of RPE cells decreased in a dose-dependent manner. After treatment with PDTC of concentration varying from 0. 062 to 1 g/L for 24 h, the PCNA expression was also suppressed in a dose-dependent manner. It is concluded that PDTC can inhibit the proliferation of RPE cells in vitro in a dose-and time-dependent manner, at least in part, by down-regulating the expression of PCNA. PDTC may be used to prevent and treat the proliferative vitreoretinopathy （PVR）.

关键词： pyrrolidine dithiocarbamate proliferative vitreoretinopathy retinal pigment epithelium cells

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The pharmacological mechanism underlying the apoptosis of human hepatic stellate cells LX-2 induced by NF-κB inhibitor PDTC

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Journal of Chinese Pharmaceutical Sciences 2022年第9期31卷 665-676页

作者： Jin Huang Kaixiang Deng Meizhen Huang Gaomin Lin Mei Lin Shuimei Lian Meiquan Zhang Department of Infection Second affiliated Hospital of Fujian University of Traditional Chinese MedicineFuzhou 350003China Department of Respiratory and Critical Care Medicine Fujian Geriatric HospitalFuzhou 350009China Department of Traditional Chinese Medicine First Hospital of Nanping CityNanping 353000China

In the present study,we aimed to confirm whether NF-κB inhibitor pyrrolidine dithiocarbamate(PDTC)could induce apoptosis of human hepatic stellate cells(HSCs)LX-2 and explore the potential pharmacological mechanism underlying these *** this study,LX-2 cells were cultured in vitro,and the experiment was divided into two groups,including the control and PDTC *** viability of LX-2 cells was measured by CCK8 assay after the cells were exposed to *** anti-apoptotic effect of PDTC was detected by AO/EB double assay staining ***,the activities of NF-κB,Fas/FasL,apoptosis-related proteins,as well as the cellular localization of AIF,were determined by Western blotting analysis and immunofluorescence staining *** PDTC treatment for 12 and 24 h,AO/EB dual staining showed typical apoptotic changes,such as cell volume reduction,cell shrinkage,nuclear fragmentation,and so *** at 60μmol/L significantly increased the proliferation inhibition rate and decreased the secretion of collagen I,collagen III,andα-SMA in LX-2 *** Western blotting analysis and RT-PCR showed no significant difference in the expression of AIF between the control group and PDTC group,and the expressions of Fas and FasL were not observed in all groups(P>0.05).Further results showed that PDTC could promote the displacement of AIF from mitochondria to the nucleus,activate the apoptotic signaling in the cell nucleus,and possibly participate in the apoptosis process of LX-2 *** conclusion,the pharmacological mechanism of PDTC against hepatic fibrosis might be to promote the displacement of AIF from mitochondria to the nucleus,then activate the apoptotic signaling in the cell nucleus,and finally induce the apoptosis of LX-2 ***,these results also revealed that the Fas/FasL-mediated apoptosis pathway was not involved in the PDTC-induced apoptosis process of LX-2 cells.

关键词： Hepatic fibrosis LX-2 Fas/FasL AIF pyrrolidine dithiocarbamate

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