Raw data of the effects of Chlorogenic acid in 3-Nitropropionic acid induced toxicity and genotoxicity.
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ABSTRACT:
SUBMITTER: Norberto AH
PROVIDER: S-EPMC5567390 | biostudies-literature | 2017 Oct
REPOSITORIES: biostudies-literature
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Raw data of the effects of Chlorogenic acid in 3-Nitropropionic acid induced toxicity and genotoxicity.
Norberto Alarcón-Herrera AH Saúl Flores-Maya FM Belén Bellido B García-Bores Ana M M Ernesto Mendoza M Guillermo Ávila-Acevedo ÁA Elizabeth Hernández-Echeagaray HE
Data in brief 20170712
The raw data showed in this article comes from the published research article entitled "Protective effects of Chlorogenic acid in 3-Nitropropionic acid induced toxicity and genotoxicity" Food Chem Toxicol. 2017 May 3. pii: S0278-6915(17)30226-0. DOI:10.1016/j.fct.2017.04.048. [1]. Data illustrates antitoxic and antigenotoxic effects of Chlorogenic acid (CGA) on toxicity and genotoxicity produced by the <i>in vivo</i> treatment with mitochondria toxin 3-Nitropropionic acid (3-NP) in mice. Toxicit ...[more]
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Project description:As the economy grows, there is a growing emphasis on food safety. The health benefits of chlorogenic acid (CGA), a common polyphenol in diets, are known, but the safe consumption dosage and potential harm to liver cells from excessive CGA are not well researched.
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Project description:CONTEXT:Triptolide (TP) has outstanding biological activities, but it induces toxicities, particular hepatotoxicity, severely limiting its clinical application. Chlorogenic acid (CGA) has prominently medicinal and nutritional values. However, until now, it is not known whether CGA could mitigate TP-induced hepatotoxicity. OBJECTIVE:This study explored the possible protection of CGA against TP-induced hepatotoxicity and its potential mechanisms, for the first time. MATERIAL AND METHODS:KM mice were treated orally with TP at a single dose of 1?mg/kg at 4?h after being treated with CGA (10, 20 and 40?mg/kg) for seven continuous days. Blood samples were collected at 24?h after TP administration for measurement of serum biomarkers, and hepatic tissues for analysis of potential mechanisms. RESULTS:TP treatment-induced acute hepatotoxicity manifested by the significant elevation in serum alanine transaminase (93.9?U/L), aspartate transaminase (185.8?U/L) and hepatic malondialdehyde (0.637??mol/mg protein), and the remarkable reduction in hepatic glutathione (1.425??g/mg protein), glutathione S-transferase, glutathione peroxidase, superoxide dismutase and catalase (91.7, 320.7, 360.6 and 140.7?U/mg protein, respectively). In contrast, pretreatment with CGA for 7?days effectively attenuated acute liver injury and oxidative stress caused by TP with each ED50 of 44.4, 57.1, 46.6, 22.2, 40.9, 58.1, 86.4 and 61.0?mg/kg, respectively. Furthermore, pretreatment with CGA promoted the accumulation of Nrf2 into the nucleus, and up-regulated mRNA expression of Nrf2-target downstream genes. DISCUSSION AND CONCLUSIONS:Combined CGA medication may probably reduce the risk of TP poisoning, and in-depth mechanisms can be developed around the signal molecules of Nrf2.
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