Theanine prevents doxorubicin-induced acute hepatotoxicity by reducing intrinsic apoptotic response

Nagai, Katsutoshi; Oda, Ayano; Konishi, Hiroki

doi:10.1016/j.fct.2015.02.009

Cited by 49 publications

(44 citation statements)

References 26 publications

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“…Oxidative stress has been reported to elicit mitochondrial-dependent (intrinsic) apoptotic pathway [43]. Induced level of ROS up regulates Bax expression leading to permeabilizing the external mitochondrial membrane, the release of cytochrome c and the activation of caspases which ultimately lead to the apoptotic degradation phase [44].…”

Section: Discussionmentioning

confidence: 99%

Melissa officinalis Protects against Doxorubicin-Induced Cardiotoxicity in Rats and Potentiates Its Anticancer Activity on MCF-7 Cells

et al. 2016

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Cardiotoxicity is a limiting factor of doxorubicin (DOX)-based anticancer therapy. Due to its beneficial effects, we investigated whether standardized extract of Melissa officinalis (MO) can attenuate doxorubicin-induced cardiotoxicity and can potentiate the efficacy of DOX against human breast cancer cells. MO was administered orally to male albino rats once daily for 10 consecutive days at doses of 250, 500 and 750 mg/kg b.wt. DOX (15 mg/kg b.wt. i.p.) was administered on the 8th day. MO protected against DOX-induced leakage of cardiac enzymes and histopathological changes. MO ameliorated DOX-induced oxidative stress as evidenced by decreasing lipid peroxidation, protein oxidation and total oxidant capacity depletion and by increasing antioxidant capacity. Additionally, MO pretreatment inhibited inflammatory responses to DOX by decreasing the expressions of nuclear factor kappa-B, tumor necrosis factor-alpha and cyclooxygenase-2 and the activity of myeloperoxidase. MO ameliorated DOX-induced apoptotic tissue damage in heart of rats. In vitro study showed that MO augmented the anticancer efficacy of DOX in human breast cancer cells (MCF-7) and potentiated oxidative damage and apoptosis. Thus, combination of DOX and MO may prove future cancer treatment protocols safer and more efficient.

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Section: Discussionmentioning

confidence: 99%

Melissa officinalis Protects against Doxorubicin-Induced Cardiotoxicity in Rats and Potentiates Its Anticancer Activity on MCF-7 Cells

et al. 2016

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“…Our previous and present studies demonstrated that theanine may protect against multi-organ injury due to DOX [15]. On the other hand, there were concerns that theanine may weaken the antitumor potency of DOX.…”

Section: Discussionmentioning

confidence: 99%

“…Control rats received physiological saline only at the same times. The dosages of DOX and theanine were selected based on the dosage settings in the previous studies [15, 16]. Rat urine was collected for 24 h from the 4th day to the 5th day.…”

Section: Methodsmentioning

confidence: 99%

Prevention of Doxorubicin-Induced Renal Toxicity by Theanine in Rats

et al. 2018

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Doxorubicin (DOX) is a highly potent anti-neoplastic agent widely used in clinical practice, but its dosage and duration of administration are strictly limited due to dose-related organ damage. In the present study, we examined whether theanine, an amino acid derivative found in green tea leaves, can protect against DOX-induced acute nephrotoxicity in rats. Decreases in the creatinine clearance by DOX administration were attenuated by concurrent treatment with theanine, which was consistent with the change in histological renal images assessed by microscopic examination. Theanine had no effect on the distribution of DOX to the kidney. The production of lipid peroxide in the kidney after DOX administration was suppressed by concurrent treatment with theanine. Reduced glutathione content, but not superoxide dismutase activity, was decreased following DOX administration, whereas this change was suppressed when theanine was given in combination with DOX. These results suggest that theanine prevents DOX-induced acute nephrotoxicity through its antioxidant properties.

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“…NF-κBp65 is predominant in the apoptotic regulation process by regulating the expression of downstream Bcl-2 genes. Bax participates in apoptotic responses via intrinsic mitochondrial-dependent signaling by inducing the release of cytochrome c (23,(43)(44)(45). Another cell death protease is caspase-3, which serves a role in cell apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Magnesium isoglycyrrhizinate ameliorates doxorubicin‑induced acute cardiac and hepatic toxicity via anti‑oxidant and anti‑apoptotic mechanisms in mice

Zhang

Song

et al. 2017

Exp Ther Med

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Abstract. The present study investigated the effects and potential mechanisms of action of magnesium isoglycyrrhizinate (MgIG) in doxorubicin (DOX)-treated mice. Histopathological analysis and western blot analysis were conducted in the liver and heart tissues and biochemical analysis of the serum was performed. The results revealed that MgIG (10, 20 and 40 mg/kg/day) could protect the structure and functions of the liver and heart by inhibiting the activities of the myocardial enzymes creatine kinase (CK), CK-MB and lactate dehydrogenase and the hepatic-specific enzymes aspirate aminotransferase and alanine aminotransferase, increasing the activities of the antioxidants superoxide dismutase and glutathione peroxidase, and inhibiting cellular apoptosis induced by DOX (30 mg/kg). These results demonstrate that inhibiting lipid peroxidation and reducing myocardial and hepatocyte apoptosis may be one of the mechanisms by which MgIG exhibits hepatoprotective and cardioprotective effects in DOX-treated mice.

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Theanine prevents doxorubicin-induced acute hepatotoxicity by reducing intrinsic apoptotic response

Cited by 49 publications

References 26 publications

Melissa officinalis Protects against Doxorubicin-Induced Cardiotoxicity in Rats and Potentiates Its Anticancer Activity on MCF-7 Cells

Melissa officinalis Protects against Doxorubicin-Induced Cardiotoxicity in Rats and Potentiates Its Anticancer Activity on MCF-7 Cells

Prevention of Doxorubicin-Induced Renal Toxicity by Theanine in Rats

Magnesium isoglycyrrhizinate ameliorates doxorubicin‑induced acute cardiac and hepatic toxicity via anti‑oxidant and anti‑apoptotic mechanisms in mice

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