Protective effects of taurine on doxorubicin-induced acute hepatotoxicity through suppression of oxidative stress and apoptotic responses

Nagai, Katsutoshi; Fukuno, Shuhei; Oda, Ayano; Konishi, Hiroki

doi:10.1097/cad.0000000000000299

Cited by 62 publications

(19 citation statements)

References 24 publications

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“…In the present study, the decrease in GSH after DOX administration was suppressed by concurrent theanine treatment, but the SOD activity was not significantly altered by DOX. In light of the findings of our previous study [22], the change in the GSH levels in the kidneys of DOX-treated rats was minor compared with that in the liver. This may be attributed to the existence of potent defense systems to eliminate ROS in the kidneys, but DOX was clearly shown to impair the renal functions by increasing oxidative stress.…”

Section: Discussionmentioning

confidence: 98%

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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Section: Discussionmentioning

confidence: 98%

Prevention of Doxorubicin-Induced Renal Toxicity by Theanine in Rats

et al. 2018

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“…Taurine, a mammalian amino acid, was shown to protect neurons from glutamate cytotoxicity, maintain MMP, and reduce ROS in SH-SY5Y cells [222]. Taurine also protected mitochondria by activating Akt-CREB-peroxisome proliferator-activated receptor gamma co-activator 1-α (PGC1α) pathway [223,224,225]. In prenatally-stressed (PS) rats that had defects in learning and memory, taurine reduced mitochondrial ROS, restored MMP, COX, ATP, and SOD2, and increased Akt-CREB signaling pathway and PGC1α expression in the hippocampi [223].…”

Section: Natural Compounds That Can Activate Nrf2 And/or Neurotropmentioning

confidence: 99%

Can Co-Activation of Nrf2 and Neurotrophic Signaling Pathway Slow Alzheimer’s Disease?

Murphy

Park

2017

IJMS

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Alzheimer’s disease (AD) is a multifaceted disease that is hard to treat by single-modal treatment. AD starts with amyloid peptides, mitochondrial dysfunction, and oxidative stress and later is accompanied with chronic endoplasmic reticulum (ER) stress and autophagy dysfunction, resulting in more complicated pathogenesis. Currently, few treatments can modify the complicated pathogenic progress of AD. Compared to the treatment with exogenous antioxidants, the activation of global antioxidant defense system via Nrf2 looks more promising in attenuating oxidative stress in AD brains. Accompanying the activation of the Nrf2-mediated antioxidant defense system that reduce the AD-causative factor, oxidative stress, it is also necessary to activate the neurotrophic signaling pathway that replaces damaged organelles and molecules with new ones. Thus, the dual actions to activate both the Nrf2 antioxidant system and neurotrophic signaling pathway are expected to provide a better strategy to modify AD pathogenesis. Here, we review the current understanding of AD pathogenesis and neuronal defense systems and discuss a possible way to co-activate the Nrf2 antioxidant system and neurotrophic signaling pathway with the hope of helping to find a better strategy to slow AD.

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“…However, DOX causes various toxic effects, the most common of which is cardiotoxicity (2). Multiple mechanisms are involved in DOX-induced cardiomyopathy, including the increase in cardiac oxidative stress, as evidenced by reactive oxygen species that induce damage such as lipid peroxidation, and changes in adenylate cyclase activity leading to apoptosis and inflammation-related signaling pathways (3,4). It has previously been suggested that DOX also elicits inflammatory effects by increasing the expression levels of nuclear factor kappa-B (NF-κB), and induces the production of various proinflammatory mediators, including tumor necrosis factor (TNF)-α (5).…”

Section: Introductionmentioning

confidence: 99%

Vitexin attenuates acute doxorubicin cardiotoxicity in rats via the suppression of oxidative stress, inflammation and apoptosis and the activation of FOXO3a

Sun

Yan

Yao

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. Doxorubicin (DOX) is one of the most effective chemotherapeutic drugs. However, its clinical use has been hampered due to the development of cardiotoxicity. Vitexin, which is the active ingredient of hawthorn leaf extract, has various biological activities, including antioxidant and anti-inflammatory actions. The present study aimed to investigate whether vitexin was able to protect against DOX-induced acute cardiotoxicity in model rats and the mechanisms of this protective effect were assessed. Adult Sprague-Dawley rats were randomly assigned into the control (saline only), model (DOX only) and vitexin-treated (DOX plus vitexin) groups. Rats in the model and vitexin-treated groups were injected with DOX (2 mg/kg; i.p.) once a week for 4 weeks. Rats in the vitexin-treated group were administered 30 mg/kg oral vitexin once daily at doses for 4 weeks. The levels of lactate dehydrogenase, creatine kinase isoenzyme-MB, malondialdehyde, superoxide dismutase, catalase and myeloperoxidase were assessed using assay kits. The levels of inflammatory mediators, including tumor necrosis factor-α, interleukin (IL)-1β, IL-6, nuclear factor (NF)-κB, and caspase-3, were assayed by the enzyme-linked immunosorbent assay method. Western blot analysis was performed to assess the protein expression levels of p-FOXO3a. Vitexin pretreatment significantly protected against DOX-induced myocardial damage, which was characterized by increased serum creatine kinase isoenzyme-MB and lactate dehydrogenase. Vitexin significantly ameliorated oxidative stress injury evoked by DOX, demonstrated by the inhibition of lipid peroxidation and the elevation of antioxidant enzyme activities. Furthermore, DOX provoked inflammatory responses by increasing the expression levels of IL-1β, IL-6, NF-κB and tumor necrosis factor-α, whereas vitexin pretreatment significantly inhibited these inflammatory responses. Notably, DOX induced apoptotic tissue damage by increasing caspase-3 activity, whereas vitexin administration was able to decrease caspase-3 activity. In addition, vitexin induced elevated FOXO3a protein expression levels in the vitexin-treated group. In conclusion, the findings of the present study suggested that vitexin possesses cardioprotective action against DOX-induced cardiotoxicity by suppressing oxidative stress, inflammation and apoptotic signals. IntroductionDoxorubicin (DOX), which belongs to the anthracyclines family, has been used to treat cancer since the late 1960s. It is a well-established and highly effective antineopalstic agent that is used to treat various adult and pediatric cancers, including solid tumors, leukemia, lymphomas and breast cancer (1). However, DOX causes various toxic effects, the most common of which is cardiotoxicity (2). Multiple mechanisms are involved in DOX-induced cardiomyopathy, including the increase in cardiac oxidative stress, as evidenced by reactive oxygen species that induce damage such as lipid peroxidation, and changes in adenylate cyclase activity leading to apoptosis and inflammation-re...

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Protective effects of taurine on doxorubicin-induced acute hepatotoxicity through suppression of oxidative stress and apoptotic responses

Cited by 62 publications

References 24 publications

Prevention of Doxorubicin-Induced Renal Toxicity by Theanine in Rats

Prevention of Doxorubicin-Induced Renal Toxicity by Theanine in Rats

Can Co-Activation of Nrf2 and Neurotrophic Signaling Pathway Slow Alzheimer’s Disease?

Vitexin attenuates acute doxorubicin cardiotoxicity in rats via the suppression of oxidative stress, inflammation and apoptosis and the activation of FOXO3a

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