Duloxetine, a Balanced Serotonin-Norepinephrine Reuptake Inhibitor, Improves Painful Chemotherapy-Induced Peripheral Neuropathy by Inhibiting Activation of p38 MAPK and NF- κB

This study not only provides biological evidence to support the use of duloxetine as the first standard CIPN drug but will also lead to potential new targets for CIPN drug development. Introduction A major dose-limiting complication of chemotherapy is chemotherapy-induced peripheral neuropathy (CIPN). The greatest contributors to CIPN are taxanes (e.g., paclitaxel) and platinum-based (e.g., oxaliplatin) treatments (Krukowski et al., 2015). Paclitaxel (PTX) can effectively treat several of the most common cancers including breast cancer, lung cancer, and ovarian cancer (Ewertz et al., 2015; Cetinkaya-Fisgin et al., 2016; Hopkins et al., 2016). Oxaliplatin (OXA), a third-generation diaminocyclohexane (DACH) platinum agent, is used as a first-line chemotherapy in combination with 5-fluorouracil to treat resectable and advanced colorectal cancer (Ta et al., 2006). However, these chemotherapy drugs can induce painful neuropathy at an incidence rate as high as 85–90%. Patients with CIPN experience sensory dysfunction including allodynia, hyperalgesia, dysesthesia, and paranaesthesia (Makker et al., 2017). These symptoms can lead to chronic disabilities that persist despite dose reduction and discontinuation of treatment. Recent studies have evaluated chemotherapy-related neuropathic pain. However, the mechanisms by which chemotherapy drugs cause neuropathy are not well understood, which severely limits development of novel therapeutic methods and drugs (Taillibert et ...
Source: Frontiers in Pharmacology - Category: Drugs & Pharmacology Source Type: research

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