Protective effects of HFE7A, mouse anti-human/mouse Fas monoclonal antibody against acute and lethal hepatic injury induced by Jo2

Yoshida, Hiroko; Watanabe, Kenji; Takahashi, Shuntaro; Ichikawa, Kimihisa

doi:10.1007/s10616-009-9244-6

Cited by 4 publications

(4 citation statements)

References 31 publications

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“…TNF‐receptor and Fas ligation are well‐characterized processes leading to massive apoptosis in various cellular models . The Fas‐mediated secretion of TNF‐α aggravates apoptosis .…”

Section: Discussionmentioning

confidence: 99%

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Alpha-1-antitrypsin inhibits acute liver failure in mice

et al. 2014

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Acute liver failure remains a critical clinical condition, with high mortality rates, and increased apoptosis of hepatocytes represents a key event in the cause of liver failure. Alpha-1-antitrypsin (AAT) is synthesized and secreted mainly by hepatocytes, and plasma purified AAT is used for augmentation therapy in patients with AAT deficiency. Because AAT therapy exerts antiinflammatory and immune modulatory activities in various experimental models, and it was recently suggested that AAT exerts antiapoptotic activities, we aimed to explore whether administration of AAT may represent a therapeutic strategy to treat acute liver failure in mice. Well-established preclinical models of acute liver failure such as the Jo2 FAS/CD95 activating model and models of acetaminophen and aamanitin poisoning were used. Therapeutic effects of AAT were evaluated by monitoring animal survival, histopathological changes, measurement of caspase activity, and serum cytokine levels. Systemic treatment with AAT significantly decreased Jo2-induced liver cell apoptosis and prolonged survival of mice. Native and oxidized (lacking elastase inhibitory activity) forms of AAT were equally effective in preventing acute liver injury and showed direct inhibition of active caspase-3 and 28 in liver homogenates and in a cell-free system in vitro. Concomitantly, mice treated with AAT showed significantly lower serum levels of tumor necrosis factor alpha (TNF-a), which also paralleled the reduced activity of ADAM17 (TACE). Noticeably, the increased survival and a reduction of apoptotic hepatocytes were also observed in the a-amanitin and acetaminophen-induced liver injury mouse models. Conclusion: Our data suggest that systemic administration of AAT can be a promising therapy to treat acute liver failure and clinical studies to explore this treatment in humans should be initiated. (HEPATOLOGY 2014;59:2299-2308

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Section: Discussionmentioning

confidence: 99%

“…TNF-receptor and Fas ligation are well-characterized processes leading to massive apoptosis in various cellular models. 21,43 The Fas-mediated secretion of TNF-a aggravates apoptosis. 2 Second, Fas activation might increase hepatic chemokines that recruit TNF-asecreting neutrophils to the liver.…”

Section: Discussionmentioning

confidence: 99%

Alpha-1-antitrypsin inhibits acute liver failure in mice

et al. 2014

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“…These include vitamins, fatty acids and antibody (Edenharder et al 1999;Rao et al 2001;Yoshida et al 2010;Turkez et al 2012b). Concomitant treatment with the anti-oxidants provided protection against oxidative damage by mutagens in experimental animals (Abubakar et al 2003;Esparza et al 2003;Geyikoglu et al 2005;.…”

Section: Introductionmentioning

confidence: 99%

Xanthoria elegans (Link) (lichen) extract counteracts DNA damage and oxidative stress of mitomycin C in human lymphocytes

2012

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Several lichen species have been used for medicinal purposes throughout the ages, and they are reported to be effective in the treatment of different disorders including ulcer and cancer. It is revealed that lichens may be easily accessible sources of natural drugs and possible food supplements after their safety evaluations. The main objective in this study was to evaluate the roles of aqueous extracts of Xanthoria elegans (at 25, 50 and 100 lg/ml) upon mitomycin C (MMC; at 10 -7 M) induced genotoxic and oxidative damages in cultured human lymphocytes. X. elegans were collected from the Erzurum and Artvin provinces (in Turkey) during August 2010. After the application of MMC and X. elegans extract (XEE), separate and together, human whole blood cultures were assessed by four genotoxicity end-points including chromosomal aberration, micronucleus, sister chromatid exchange (SCE) and 8-oxo-2-deoxyguanosine (8-OHdG) assays. In addition, biochemical parameters [total antioxidant capacity (TAC) and total oxidative stress (TOS)] were examined to determine oxidative effects. According to our results, the frequencies of cytogenetic endpoints and 8-OH-dG levels were significantly increased by MMC compared with controls in human peripheral lymphocytes. MMC caused oxidative stress by altering TAC and TOS levels. On the contrary, XEE led to increases of TAC level without changing TOS level. XEE had no genotoxic effect. Furthermore, our findings revealed that MMC induced increases in the mean frequencies of four genotoxic indices were diminished by XEE in dose dependent manner, indicating its protective role towards cells from MMC exerted injury. In conclusion, the results obtained in the present study indicate for the first time that XEE is a potential source of natural antigenotoxicants.

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“…Recently, extensive efforts were made to investigate therapeutic substances capable of reducing the genotoxicity of various natural and man-made mutagens in human life Turkez and Geyikoglu 2010b). Also, these include antibody, fatty acids, minerals and vitamins (Edenharder et al 1999;Rao et al 2001;Yoshida et al 2010;Turkez et al 2012a, b, c, d). Concomitant treatment with antioxidants provided protection against oxidative damage by mutagens in experimental animals (Abubakar et al 2003;Esparza et al 2003;Geyikoglu et al 2005;Turkez and Geyikoglu 2010a).…”

Section: Introductionmentioning

confidence: 99%

In vitro studies on protective effect of Glycyrrhiza glabra root extracts against cadmium-induced genetic and oxidative damage in human lymphocytes

Dirican

Türkez

2013

Cytotechnology

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Cadmium is a modern environmental contaminant that is toxic and carcinogenic. Glycyrrhiza glabra is a traditional medicinal herb which grows in the various parts of the World. Recent studies demonstrated that G. glabra has antifungal, antimicrobial, antioxidant, and powerful antiinflammatory features. The purpose of this study was to investigate the genetic safety of extracts from G. glabra and its effects on cadmium (as CdCl 2 ) induced genotoxicity. Therefore we evaluated the capability of G. glabra extract to inhibit the rate of micronucleus (MN), sister chromatid exchange (SCE) formations induced by CdCl 2 . Moreover, to assess the effects of G. glabra on cell viability and oxidative status, we performed 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) and total antioxidant capacity (TAC) assays. Our results showed that there were significant increases (P \ 0.05) in both SCE and MN frequencies of cultures treated with CdCl 2 (5 ppm) as compared to controls. However, co-application of G. glabra extract (5, 10 and 20 ppm) and CdCl 2 resulted in decreases of MN and SCE rates as compared to the group treated with CdCl 2 alone. Again, the results of MTT and TAC assays clearly indicated dose dependent ameliorative effects of G. glabra extracts against CdCl 2 toxicity. In conclusion, this study demonstrated for the first time that G. glabra extracts provided increased resistance of DNA against CdCl 2 induced genetic and oxidative damage in human lymphocytes. So, the risk on target tissues of CdCl 2 could be reduced and ensured early recovery from its toxicity.

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Protective effects of HFE7A, mouse anti-human/mouse Fas monoclonal antibody against acute and lethal hepatic injury induced by Jo2

Abstract: HFE7A is a mouse anti-human/mouse Fas monoclonal antibody which, protects mice from fulminant hepatitis induced by Jo2. Herein, we report on the mechanism of the protective effect of HFE7A against Jo2-induced acute and lethal hepatic injury.

Cited by 4 publications

References 31 publications

Alpha-1-antitrypsin inhibits acute liver failure in mice

Alpha-1-antitrypsin inhibits acute liver failure in mice

Xanthoria elegans (Link) (lichen) extract counteracts DNA damage and oxidative stress of mitomycin C in human lymphocytes

In vitro studies on protective effect of Glycyrrhiza glabra root extracts against cadmium-induced genetic and oxidative damage in human lymphocytes

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