Telmisartan ameliorates cisplatin-induced nephrotoxicity by inhibiting MAPK mediated inflammation and apoptosis

Malik, Salma; Suchal, Kapil; Gamad, Nanda; Dinda, Amit Kumar; Arya, Dharamvir Singh; Bhatia, Jagriti

doi:10.1016/j.ejphar.2014.12.008

Cited by 106 publications

(72 citation statements)

References 29 publications

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“…The MAPK pathway is an important signal transduction pathway that links extracellular signals to intracellular processes and is highly associated with apoptosis and inflammation. 35 We found that JNK and p38 MAPK were both phosphorylated in response to exposure to 0.05-μm microbeads. In the copepod T. japonicus, p38 MAPK has been shown to be activated in response to ultraviolet B (UVB) radiation and copper exposure.…”

Section: Environmental Science and Technologymentioning

confidence: 89%

Microplastic Size-Dependent Toxicity, Oxidative Stress Induction, and p-JNK and p-p38 Activation in the Monogonont Rotifer (Brachionus koreanus)

Jeong

Won

Kang

et al. 2016

Environ. Sci. Technol.

1,004

341

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In this study, we evaluated accumulation and adverse effects of ingestion of microplastics in the monogonont rotifer (Brachionus koreanus). The dependence of microplastic toxicity on particle size was investigated by measuring several in vivo end points and studying the ingestion and egestion using 0.05-, 0.5-, and 6-μm nonfunctionalized polystyrene microbeads. To identify the defense mechanisms activated in response to microplastic exposure, the activities of several antioxidant-related enzymes and the phosphorylation status of mitogen-activated protein kinases (MAPKs) were determined. Exposure to polystyrene microbeads of all sizes led to significant sizedependent effects, including reduced growth rate, reduced fecundity, decreased lifespan and longer reproduction time. Rotifers exposed to 6-μm fluorescently labeled microbeads exhibited almost no fluorescence after 24 h, while rotifers exposed to 0.05-and 0.5-μm fluorescently labeled microbeads displayed fluorescence until 48 h, suggesting that 6-μm microbeads are more effectively egested from B. koreanus than 0.05-or 0.5-μm microbeads. This observation provides a potential explanation for our findings that microbead toxicity was sizedependent and smaller microbeads were more toxic. In vitro tests revealed that antioxidant-related enzymes and MAPK signaling pathways were significantly activated in response to microplastic exposure in a size-dependent manner.

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Section: Environmental Science and Technologymentioning

confidence: 89%

Microplastic Size-Dependent Toxicity, Oxidative Stress Induction, and p-JNK and p-p38 Activation in the Monogonont Rotifer (Brachionus koreanus)

Jeong

Won

Kang

et al. 2016

Environ. Sci. Technol.

1,004

341

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“…It is recognized that oxidative stress acts as an important pathogenic factor in causing cisplatin-induced acute kidney injury (Malik et al, 2015;Hagar et al, 2015). Normally, inside the cell, mitochondria produce ROS such as superoxides, hydroxyl and hydrogen peroxide regularly via electron transport chain but they are also simultaneously scavenged by anti-oxidant enzymessuperoxide dismutase, glutathione-s-transferase, catalase and glutathione peroxidase (Richter et al, 1995).…”

Section: Discussionmentioning

confidence: 99%

“…We observed that cisplatin at the dose of 8 mg/kg; i.p. was found to be the most optimum dose for inducing nephrotoxicity in rats and this dose of cisplatin was subsequently used to induce nephrotoxicity in rats (Malik et al, 2015).…”

Section: Experimental Protocolmentioning

confidence: 99%

Nobiletin ameliorates cisplatin-induced acute kidney injury due to its anti-oxidant, anti-inflammatory and anti-apoptotic effects

Malik

Bhatia

Suchal

et al. 2015

Experimental and Toxicologic Pathology

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“…18,24,25 Inside the tubular cells, cisplatin is aquated into a highly reactive electrophile, which rapidly reacts with thiol-containing molecules including glutathione. It also induces mitochondrial dysfunction and increases ROS production by disrupting the respiratory chain.…”

Section: Discussionmentioning

confidence: 99%

“…This dose (8 mg/kg) of cisplatin was selected on the basis of its efficacy in causing nephrotoxicity in rats. 18 In all the groups, all the animals were anaesthetized with pentobarbitone sodium (60 mg/kg; i.p.) on the 10th day of treatment.…”

Section: Methodsmentioning

confidence: 99%

Molecular mechanisms underlying attenuation of cisplatin-induced acute kidney injury by epicatechin gallate

Malik

Suchal

Bhatia

et al. 2016

Laboratory Investigation

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Cisplatin, a platinum compound, is used as a first-line agent against various forms of solid cancers. Nephrotoxicity is an important adverse effect of cisplatin therapy, which involves increased oxidative stress, inflammation, apoptosis, and activation of the mitogen-activated protein kinase (MAPK) pathway. It is well known that the bioactive compounds present in green tea are used to treat various disorders due to their biological activities. With this background, the present study was aimed to investigate the effect of epicatechin gallate (ECG), a green tea polyphenol, in cisplatin-induced nephrotoxicity in rats. To achieve this, ECG (1.25, 2.5, and 5 mg/kg; intraperitoneal (i.p.)) was administered to male albino Wistar rats for the period of 10 days. On the 7th day, a single i.p. injection of cisplatin (8 mg/kg) was injected into rats to produce kidney injury and the animals were then killed on the 10th day. Cisplatin toxicity was associated with enhanced oxidative stress, impaired renal function along with marked tubular necrosis in Histopathology. Furthermore, cisplatin activated the MAPK pathway, which contributed to inflammation and apoptosis in the kidney of treated rats. In contrast, ECG (5 mg/kg) pretreatment normalized cisplatin-induced oxidative stress, renal function, and histopathological changes. ECG also prevented the activation of the MAPK pathway, and attenuated inflammation and apoptosis in rats. These findings suggest that ECG prevented cisplatin-induced oxidative stress, inflammation, and apoptosis by downregulating the MAPK pathway and resulted in improved renal function.

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Telmisartan ameliorates cisplatin-induced nephrotoxicity by inhibiting MAPK mediated inflammation and apoptosis

Cited by 106 publications

References 29 publications

Microplastic Size-Dependent Toxicity, Oxidative Stress Induction, and p-JNK and p-p38 Activation in the Monogonont Rotifer (Brachionus koreanus)

Microplastic Size-Dependent Toxicity, Oxidative Stress Induction, and p-JNK and p-p38 Activation in the Monogonont Rotifer (Brachionus koreanus)

Nobiletin ameliorates cisplatin-induced acute kidney injury due to its anti-oxidant, anti-inflammatory and anti-apoptotic effects

Molecular mechanisms underlying attenuation of cisplatin-induced acute kidney injury by epicatechin gallate

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