Protective effect of alpha lipoic acid on cisplatin induced hepatotoxicity in rats

Pınar, Neslihan; Çakırca, Gökhan; Hakverdı, Sibel; Kaplan, Mahir

doi:10.1080/10520295.2019.1667025

Cited by 13 publications

(14 citation statements)

References 23 publications

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“…However, the effect of MOR use in conjunction with CP on the liver has not yet been clarified. The current study showed that CP caused deterioration in the function and the structure of the liver, as well as induced hepatic oxidative stress, which was expected from previous studies [3,6]. Similar findings have been shown with MOR alone, which was also in line with previous results [17][18][19].…”

Section: Discussionsupporting

confidence: 93%

“…Here, the present study showed for the first time that MOR/CP combination enhanced of hepatic inflammation by inducing TNF-α/IL-6 pathway. The present study also showed that CP induced apoptosis by up-regulating caspase 3, which was expected from previous studies [3,6,23]. MOR alone also up-regulated caspase 3 in the liver.…”

Section: Discussionsupporting

confidence: 91%

“…In addition, several pro-inflammatory cytokines have been shown to increase after CP treatment [3,4], suggesting a strong role of inflammation as a mechanistic process in CP-induced hepatotoxicity. Administration of CP was also reported to induce hepatic programmed cell death as evident by up-regulating a number of pro-apoptotic markers [5,6].…”

Section: Introductionmentioning

confidence: 98%

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P-Glycoprotein/ABCB1 Might Contribute to Morphine/Cisplatin-Induced Hepatotoxicity in Rats

El-Sheikh

2020

Sci. Pharm.

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To investigate combined effect of the anticancer drug cisplatin (CP) and the opiate analgesic morphine (MOR) on liver, rats were administered MOR (10 mg/kg/day i.p. for 10 days), with or without CP (7.5 mg/kg i.p. once at day 5 of the study). MOR or CP alone caused deterioration of liver function tests and induced damage to histological architecture of liver. In addition, each drug alone caused hepatic oxidative stress, as evident by significant increase of malondialdehyde and nitric oxide, as well as the significant decrease in GSH, catalase and SOD compared to control. Administration of either MOR or CP also caused liver inflammation, evident by the increase in the pro-inflammatory cytokines; TNF-α and IL-6. In addition, either MOR or CP induced liver apoptosis, as shown by significant increase in expression of the pro-apoptotic marker; caspase 3 compared to control. Either MOR or CP also caused up-regulation of the efflux transporter P-glycoprotein (P-gp). Combining MOR with CP caused deterioration in all parameters tested compared to CP alone. Thus, treatment with MOR worsened CP-induced hepatotoxicity through oxidative stress, inflammation and apoptosis mechanisms. In addition, both drugs contributed to the up-regulation of P-gp, which might be a new mechanism for their hepatotoxic effects.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 98%

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P-Glycoprotein/ABCB1 Might Contribute to Morphine/Cisplatin-Induced Hepatotoxicity in Rats

El-Sheikh

2020

Sci. Pharm.

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“…One of the underlying mechanisms of CP‐induced liver injury is a state of oxidative stress. [ 8 ] It is well known that CP causes reactive oxygen species (ROS) production leading to oxidative damage to the biological molecules like DNA, proteins, and lipids [ 31,34 ] therefore, the antioxidant defense system is crucial in facing oxidative stress produced and defending the cell from the dangerous effects of ROS and oxidative damage. [ 31 ] In this context, CP induced a marked rise in hepatic MDA and NO contents along with a marked decline of the antioxidant enzymes like SOD and CAT as well as the nonenzymatic antioxidant GSH hepatic levels and several studies agreed with the results of this study.…”

Section: Discussionmentioning

confidence: 99%

“…[ 31 ] In this context, CP induced a marked rise in hepatic MDA and NO contents along with a marked decline of the antioxidant enzymes like SOD and CAT as well as the nonenzymatic antioxidant GSH hepatic levels and several studies agreed with the results of this study. [ 32,34,35 ]…”

Section: Discussionmentioning

confidence: 99%

Hepatoprotective effect of arjunolic acid against cisplatin‐induced hepatotoxicity: Targeting oxidative stress, inflammation, and apoptosis

Sherif

2021

J Biochem & Molecular Tox

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Minimizing the adverse effects of chemotherapeutic agents remains a therapeutic challenge. Cisplatin (CP) induces hepatotoxicity through activation of oxidative stress, inflammation, and apoptosis cascades which is considered a significant drawback. Thus, this study aimed to highlight the possible hepatoprotective role of arjunolic acid (Arj) in a rat model of CP‐induced hepatotoxicity. Four groups of rats were included; the normal control group, Arj control group, CP group which was injected with 7.5 mg/kg CP intraperitoneally to induce hepatotoxicity, and the treated group (Arj + CP), which was orally administered 20 mg/kg Arj for 10 days with a CP hepatotoxic dose on day 5. Blood and liver tissues were assembled for analysis at the end of the study. Pretreatment with Arj exhibited a marked improvement in liver function as well as histopathology when compared with the CP group. Moreover, Arj suppressed the oxidative stress in hepatic tissue by significantly decreasing malondialdehyde and nitric oxide contents along with markedly elevating the levels of superoxide dismutase, catalase, and reduced glutathione when compared with CP injected rats. Attenuation of hepatic inflammation and apoptosis was also reported with Arj treatment through the marked reduction in the proinflammatory cytokine tumor necrosis factor α level as well as the apoptotic marker caspase‐3 protein expression in comparison to the CP group. This study explored for the first time the Arj hepatoprotective effect against CP‐induced hepatotoxicity through its antioxidant, anti‐inflammatory, and antiapoptotic activities.

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Oxoplatin‐Based Pt(IV) Lipoate Complexes and Their Biological Activity

Liu

Barth

Cseh

et al. 2022

Chemistry & Biodiversity

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α-Lipoic acid, known for its anti-inflammatory and antioxidant activity, represents a promising ligand for Pt(IV) prodrugs. Three new Pt(IV) lipoate complexes were synthesized and characterized by NMR spectroscopy ( 1 H, 13 C, 195 Pt), mass spectrometry and elemental analysis. Due to the low solubility of the complex containing two axial lipoate ligands, further experiments to examine the biological activity were performed with two Pt(IV) complexes containing just one axial lipoate ligand. Both complexes exhibit anticancer activity and produce reactive oxygen species (ROS) in the cell lines tested. Especially, the monosubstituted complex can be reduced by ascorbic acid and forms adducts with 9-methylguanine (9MeG), which is favorable for the formation of DNA-crosslinks in the cells.

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Protective effect of alpha lipoic acid on cisplatin induced hepatotoxicity in rats

Cited by 13 publications

References 23 publications

P-Glycoprotein/ABCB1 Might Contribute to Morphine/Cisplatin-Induced Hepatotoxicity in Rats

P-Glycoprotein/ABCB1 Might Contribute to Morphine/Cisplatin-Induced Hepatotoxicity in Rats

Hepatoprotective effect of arjunolic acid against cisplatin‐induced hepatotoxicity: Targeting oxidative stress, inflammation, and apoptosis

Oxoplatin‐Based Pt(IV) Lipoate Complexes and Their Biological Activity

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