Oxidative stress-mediated hepatotoxicity in rats induced by ethanol extracts of different parts of Chloranthus serratus

Context Chloranthus serratus (Thunb.) Roem. et Schult. (Chloranthaceae) is an herb widely used as a folk medicine treating inflammatory diseases, although it is toxic. Objective To investigate hepatotoxicity and related mechanisms induced by ethanol extracts of different parts of C. serratus in rats...

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Main Authors: Shuping Sun, Yang Wang, Yunyan Du, Qi Sun, Lijuan He, Enze Zhu, Jiarong Li
Format: Article
Language:English
Published: Taylor & Francis Group 2020-01-01
Series:Pharmaceutical Biology
Subjects:
Online Access:http://dx.doi.org/10.1080/13880209.2020.1859552
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author Shuping Sun
Yang Wang
Yunyan Du
Qi Sun
Lijuan He
Enze Zhu
Jiarong Li
author_facet Shuping Sun
Yang Wang
Yunyan Du
Qi Sun
Lijuan He
Enze Zhu
Jiarong Li
author_sort Shuping Sun
collection DOAJ
description Context Chloranthus serratus (Thunb.) Roem. et Schult. (Chloranthaceae) is an herb widely used as a folk medicine treating inflammatory diseases, although it is toxic. Objective To investigate hepatotoxicity and related mechanisms induced by ethanol extracts of different parts of C. serratus in rats. Materials and methods Sprague Dawley rats were divided into control (Con), ethanol extract of roots (ER), stems (ES), and leaves (EL) groups, and acute oral toxicity studies were conducted. The rats received doses of 4.14, 3.20, and 1.16 g/kg/d extracts for 14 days, respectively. Liver index, liver function and oxidative stress biomarkers, liver pathology, ultrastructure, TNF-α, ICAM-1, and Nrf2/HO-1 proteins expression levels were determined. Results The LD50 of ER, ES, and EL were higher than 10.35, 8.05, and 2.90 g/kg/p.o., respectively. The liver indexes in the extract groups increased significantly. EL dramatically increased TP, GLB, AST, ALT, ALP, TBA, MDA, ICAM-1, and TNF-α levels (p < 0.01), and induced the most obvious pathological and ultrastructural changes. ES and EL obviously decreased the T-SOD, GSH, CAT, and CHOL levels. Nrf2 and HO-1 proteins expression was reduced significantly in ES (0.77 ± 0.06, 2.33 ± 0.20) and EL (0.23 ± 0.04, 2.14 ± 0.16) groups, and reduced slightly in ER (1.08 ± 0.10; 3.39 ± 0.21) group. Discussion and conclusion ES and EL induce stronger hepatotoxicity than ER through oxidative stress and the Nrf2/HO-1 pathway, and the root is a better medicinal part, which provides a basis for clinical research, safe applications, and reasonable development of C. serratus.
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spelling doaj.art-e4704e9cc1aa45e6b02e9a3058ae9c102022-12-21T22:51:00ZengTaylor & Francis GroupPharmaceutical Biology1388-02091744-51162020-01-015811286129810.1080/13880209.2020.18595521859552Oxidative stress-mediated hepatotoxicity in rats induced by ethanol extracts of different parts of Chloranthus serratusShuping Sun0Yang Wang1Yunyan Du2Qi Sun3Lijuan He4Enze Zhu5Jiarong Li6College of Pharmacy, Wannan Medical CollegeCollege of Pharmacy, Wannan Medical CollegeCollege of Pharmacy, Wannan Medical CollegeCollege of Pharmacy, Heilongjiang University Of Chinese MedicineCollege of Pharmacy, Wannan Medical CollegeCollege of Pharmacy, Wannan Medical CollegeCollege of Pharmacy, Wannan Medical CollegeContext Chloranthus serratus (Thunb.) Roem. et Schult. (Chloranthaceae) is an herb widely used as a folk medicine treating inflammatory diseases, although it is toxic. Objective To investigate hepatotoxicity and related mechanisms induced by ethanol extracts of different parts of C. serratus in rats. Materials and methods Sprague Dawley rats were divided into control (Con), ethanol extract of roots (ER), stems (ES), and leaves (EL) groups, and acute oral toxicity studies were conducted. The rats received doses of 4.14, 3.20, and 1.16 g/kg/d extracts for 14 days, respectively. Liver index, liver function and oxidative stress biomarkers, liver pathology, ultrastructure, TNF-α, ICAM-1, and Nrf2/HO-1 proteins expression levels were determined. Results The LD50 of ER, ES, and EL were higher than 10.35, 8.05, and 2.90 g/kg/p.o., respectively. The liver indexes in the extract groups increased significantly. EL dramatically increased TP, GLB, AST, ALT, ALP, TBA, MDA, ICAM-1, and TNF-α levels (p < 0.01), and induced the most obvious pathological and ultrastructural changes. ES and EL obviously decreased the T-SOD, GSH, CAT, and CHOL levels. Nrf2 and HO-1 proteins expression was reduced significantly in ES (0.77 ± 0.06, 2.33 ± 0.20) and EL (0.23 ± 0.04, 2.14 ± 0.16) groups, and reduced slightly in ER (1.08 ± 0.10; 3.39 ± 0.21) group. Discussion and conclusion ES and EL induce stronger hepatotoxicity than ER through oxidative stress and the Nrf2/HO-1 pathway, and the root is a better medicinal part, which provides a basis for clinical research, safe applications, and reasonable development of C. serratus.http://dx.doi.org/10.1080/13880209.2020.1859552chloranthaceaeliver damagepathological changesoxidative damagetoxic mechanismnrf2/ho-1 pathway
spellingShingle Shuping Sun
Yang Wang
Yunyan Du
Qi Sun
Lijuan He
Enze Zhu
Jiarong Li
Oxidative stress-mediated hepatotoxicity in rats induced by ethanol extracts of different parts of Chloranthus serratus
Pharmaceutical Biology
chloranthaceae
liver damage
pathological changes
oxidative damage
toxic mechanism
nrf2/ho-1 pathway
title Oxidative stress-mediated hepatotoxicity in rats induced by ethanol extracts of different parts of Chloranthus serratus
title_full Oxidative stress-mediated hepatotoxicity in rats induced by ethanol extracts of different parts of Chloranthus serratus
title_fullStr Oxidative stress-mediated hepatotoxicity in rats induced by ethanol extracts of different parts of Chloranthus serratus
title_full_unstemmed Oxidative stress-mediated hepatotoxicity in rats induced by ethanol extracts of different parts of Chloranthus serratus
title_short Oxidative stress-mediated hepatotoxicity in rats induced by ethanol extracts of different parts of Chloranthus serratus
title_sort oxidative stress mediated hepatotoxicity in rats induced by ethanol extracts of different parts of chloranthus serratus
topic chloranthaceae
liver damage
pathological changes
oxidative damage
toxic mechanism
nrf2/ho-1 pathway
url http://dx.doi.org/10.1080/13880209.2020.1859552
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