This study examines the potential efficacy of acetyl-L-carnitine (ALC) to prevent and treat paclitaxel-induced pain. Rats received four intraperitoneal (i.p.) injections of 2 mg/kg paclitaxel on alternate days which, following a short delay induced marked mechanical hypersensitivity. Daily administration of ALC (50 mg/kg and 100 mg/kg; p.o.; concurrently with paclitaxel and for 14 days afterwards) prevented the development of paclitaxel-induced pain. This effect was long lasting, for at least 3 weeks after the last dose of ALC. In a separate experiment, daily administration of ALC (100 mg/kg; p.o.; for 10 days) to rats with established paclitaxel-induced pain produced an analgesic effect. This effect dissipated shortly after ALC treatment was withdrawn. We conclude that ALC may be useful in the prevention and treatment of chemotherapy-induced painful peripheral neuropathy.
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http://dx.doi.org/10.1016/j.neulet.2005.12.013 | DOI Listing |
Metabolites
December 2024
Department of Physiology, College of Korean Medicine, Kyung Hee University, Seoul 02453, Republic of Korea.
Background: Paclitaxel is a widely used anticancer drug for ovarian, lung, breast, and stomach cancers; however, its clinical use is often limited by the side effects of peripheral neuropathy. This study evaluated the effects of () extract and its active metabolite, α-cyperone, on paclitaxel-induced neuropathic pain.
Methods: The oral administration of extract at doses of 500 mg/kg and intraperitoneal administration of α-cyperone at doses of 480 and 800 μg/kg prevented both the development of cold and mechanical pain.
Adv Sci (Weinh)
December 2024
Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Institute of Neuroscience, Translational Medicine Institute, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, 710061, P. R. China.
Chemotherapeutic agents, such as paclitaxel (PTX), induce neuroplastic changes and alter gene expression in the prefrontal cortex (PFC), which may be associated with chemotherapy-induced pain and negative emotions. Notably, DNA methylation undergoes adaptive changes in neurological disorders, emerging as a promising target for neuromodulation. In this study, systemic administration of PTX leads to a decrease in the expression of the DNA methyltransferase DNMT3a, while concurrently upregulating the expression of Gabrb1 mRNA and its encoded GABARβ1 protein in the medial PFC (mPFC) of male mice.
View Article and Find Full Text PDFSci Transl Med
December 2024
Department of Cell Biology, Neurobiology, and Anatomy, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
Recent work demonstrates that epidermal keratinocytes are critical for normal touch sensation. However, it is unknown whether keratinocytes contribute to touch-evoked pain and hypersensitivity after tissue injury. Here, we used a mouse model of paclitaxel treatment to determine the extent to which keratinocyte activity contributes to the severe neuropathic pain that accompanies chemotherapy.
View Article and Find Full Text PDFNeuropharmacology
December 2024
Program in Neuroscience, Indiana University, Bloomington, IN, USA; Department of Psychological and Brain Sciences, Indiana University, Bloomington, IN, USA; Gill Institute for Neuroscience, Indiana University, Bloomington, IN, USA. Electronic address:
Cannabinoid CB agonists show promise as analgesics because they lack unwanted side effects associated with direct activation of CB receptors. CB receptor activation suppresses pathological pain in animal models, but the types of pain that best respond to CB agonists are incompletely understood. This gap in knowledge may contribute to failures in clinical translation.
View Article and Find Full Text PDFJ Pain Res
November 2024
Department of Clinical Laboratory Science, College of Health Sciences, Catholic University of Pusan, Busan, 46252, Republic of Korea.
Background: Paclitaxel (PTX) can induce chemotherapy-induced peripheral neuropathy (CIPN) as a side effect. The aim of this study was to understand the neurochemical changes induced by NGF/TrkA signaling in PTX-induced neuropathic pain.
Methods: The PTX-induced CIPN mouse model was evaluated using nerve conduction velocity (NCV) and behavioral tests.
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