Hyperin protects against cisplatin-induced liver injury in mice

Niu, Chengwei; Ma, Man; Han, Xiao; Wang, Zimin; Li, Hangyan

doi:10.1590/s0102-865020170080000005

Cited by 37 publications

(23 citation statements)

References 29 publications

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“…Whilst, both groups II and III showed; a highly significant increase P<0.01 in the concentrations of BUN, creatinine, and urea, respectively. The current findings were similar to those of (51,52). The biochemical changes in the current study may be due to that the drug causes a reduction in the glutathione concentration (which plays an important role in removing many toxic metabolites) in the tissue of the maternal liver, kidneys, and that seems to have the main role in disturbing the cellular antioxidant regulation.…”

Section: Discussionsupporting

confidence: 85%

Histopathological and some biochemical effects of platinum drug on the liver and kidney of pregnant mice Mus musculus and their embryos

Barwarei¹,

Sadoon²

2020

IJVS

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The current study was done to investigate the effects of two doses 3and 6 mg/kg B.w. of the Platinum drug on the structure of the liver and kidney of pregnant mice, and embryos in addition to the weight of the mothers, embryos, maternal liver and kidneys, as well as some biochemical parameters, were established. For this study, thirty pregnant mice were used, divided into three groups (10 mice/group) as follows; group I (control group); animals were injected intraperitoneally (IP) with distilled water on the days 7th, 12th, and 17th of gestation. The other both groups II, and III were injected intraperitoneally (IP) with the selected doses above of the Platinum at the days 7th, 12th, and 17th of gestation, respectively. Microscopically, maternal and fetal' liver sections of group II revealed vacuolation, swelling, apoptosis, infiltration of inflammatory cells, congestion, degeneration, and presence of the extramedullary hematopoietic cells, respectively. Previous lesions were increased in group III. Maternal and, fetal kidney sections of group II revealed degeneration, expansion of Bowman's space, inflammatory cells infiltration into interstitial tissue, and blood capillaries congestion. However, the previous lesions showed more severity in group III. The drug caused a reduction in the body weight of the mothers, selected organs, and embryos. Biochemical assessment of the maternal serum AST, ALT, and ALP levels showed an increase in both experimental groups II and III, but to varying degrees. Moreover, both groups II and III showed an increase in the levels of the maternal BUN and, urea. Whist, group III showed a significant increase of the creatinine compared to the control group. In conclusion, using anticancer drugs during pregnancy will harm both mothers and fetal organs. The risk of these medications represents their ability to cross the placenta and enters the fetal body. Therefore, the drug may affect the formation of the fetal organs. The drug also alters the regulatory antioxidant mechanism in the maternal body during the treatment duration. The drug should be used under medical follow up.

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Section: Discussionsupporting

confidence: 85%

Histopathological and some biochemical effects of platinum drug on the liver and kidney of pregnant mice Mus musculus and their embryos

Barwarei¹,

Sadoon²

2020

IJVS

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“…GSH-Px is an important enzyme that catalyzes the decomposition of hydrogen peroxide, which in turn, protects cell membranes and prevents cell damage [ 32 ]. MDA is a metabolite of lipid peroxidation; a high content of MDA accumulates in the body after liver injury [ 33 ]. In this study, we found that PLT could significantly regulate the levels of SOD, GSH-Px, and MDA in the body caused by liver injury, thereby protecting the liver from the effects of carbon tetrachloride.…”

Section: Discussionmentioning

confidence: 99%

Polyphenols in Liubao Tea Can Prevent CCl4-Induced Hepatic Damage in Mice through Its Antioxidant Capacities

Pan

Long

et al. 2018

Nutrients

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The present study investigated the preventive effect of polyphenols in Liubao tea (PLT) on carbon tetrachloride (CCl4)-induced liver injury in mice. The mice were initially treated with PLT, followed by induction of liver injury using 10 mL/kg CCl4. Then liver and serum indices, as well as the expression levels of related messenger RNAs (mRNAs) and proteins in liver tissues were measured. The results showed that PLT reduces the liver quality and indices of mice with liver injury. PLT also downregulates aspartate aminotransferase (AST), alanine aminotransferase (ALT), triglycerides (TGs), and malondialdehyde (MDA), and upregulates superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in the sera of mice with liver injury. PLT also reduces serum levels of interleukin-6 (IL-6), interleukin-12 (IL-12), tumor necrosis factor-α (TNF-α), and interferon-γ (IFN-γ) cytokines in mice with liver injury. Pathological morphological observation also shows that PLT reduces CCl4-induced central venous differentiation of liver tissues and liver cell damage. Furthermore, qPCR and Western blot also confirm that PLT upregulates the mRNA and protein expressions of Gu/Zn-SOD, Mn-SOD, catalase (CAT), GSH-Px, and nuclear factor of κ-light polypeptide gene enhancer in B-cells inhibitor-α (IκB-α) in liver tissues, and downregulates the expression of cyclooxygenase 2 (COX-2) and nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB). Meanwhile, PLT also raised the phosphorylated (p)-NF-κB p65 and cytochrome P450 reductase protein expression in liver injury mice. The components of PLT include gallic acid, catechin, caffeine, epicatechin (EC), epigallocatechin gallate (EGCG), gallocatechin gallate (GCG), and epicatechin gallate (ECG), which possibly have a wide range of biological activities. Thus, PLT imparts preventive effects against CCl4-induced liver injury, which is similar to silymarin.

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“…Within the cell, the hydrolysis of CP generates positively charged toxic platinum ions, which preferentially accumulate within the negatively charged mitochondria and lead to the overproduction of reactive oxygen species (ROS). [ 9,10 ] This consequently suppresses oxidative phosphorylation, as well as the activities of antioxidant enzymes, thus contributing to mitochondrial dysfunction. [ 6 ]…”

Section: Introductionmentioning

confidence: 99%

Epigallocatechin gallate and coenzyme Q10 attenuate cisplatin‐induced hepatotoxicity in rats via targeting mitochondrial stress and apoptosis

Fatima

Suhail

Alrashed

et al. 2021

J Biochem & Molecular Tox

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Despite the extensive use of cisplatin (CP) as a chemotherapeutic agent, its clinical use is often restricted by undesirable side effects, such as toxicity to normal tissues. The aim of this study was to probe the effect of a combinatorial treatment of low multiple doses of antioxidants on CP‐induced toxicity and the mitochondrial apoptotic pathway in hepatocytes. Animals received a single toxic dose of CP (7.5 mg/kg body weight) with or without combined multiple doses of epigallocatechin gallate (EGCG) and coenzyme Q10 (CoQ10) (15 and 5 mg/kg body weight, respectively). CP‐treated animals showed altered biochemical parameters, denoting hepatotoxicity, which was markedly improved by the multidose treatment with EGCG + CoQ10. The increased levels of oxidants found in the cytosolic and mitochondrial fractions isolated from the liver of CP‐administered rats were significantly attenuated by the combinatorial doses of antioxidants. EGCG + CoQ10 ameliorated the CP‐induced compromised antioxidant defenses, oxidative modification of macromolecules, decreased activities of respiratory chain enzymes, altered membrane depolarization, and swelling of liver mitochondria. Furthermore, EGCG + CoQ10 treatment inhibited CP‐induced apoptosis by suppressing the activation and mitochondrial accumulation of proapoptotic proteins and preventing the inhibition of antiapoptotic protein expression, cytochrome c efflux, caspase‐3 activation, and DNA fragmentation. Histological findings further confirmed the protective effects of EGCG + CoQ10 against CP‐induced cellular injury. Our findings revealed that the combination of EGCG and CoQ10, owing to their individual antioxidant properties, can be an effective remedy, which by maintaining redox hemostasis attenuate the mitochondrial stress‐mediated molecular and cellular processes involved in CP‐induced liver toxicity and cell death.

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Hyperin protects against cisplatin-induced liver injury in mice

Cited by 37 publications

References 29 publications

Histopathological and some biochemical effects of platinum drug on the liver and kidney of pregnant mice Mus musculus and their embryos

Histopathological and some biochemical effects of platinum drug on the liver and kidney of pregnant mice Mus musculus and their embryos

Polyphenols in Liubao Tea Can Prevent CCl4-Induced Hepatic Damage in Mice through Its Antioxidant Capacities

Epigallocatechin gallate and coenzyme Q10 attenuate cisplatin‐induced hepatotoxicity in rats via targeting mitochondrial stress and apoptosis

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