Cerebrospinal Fluid Oxaliplatin Contributes to the Acute Pain Induced by Systemic Administration of Oxaliplatin

Huang, Zhenzhen; Li, Dai; Ouyang, Handong; Liu, Cuicui; Liu, Xian-Guo; Ma, Chao; Wei, Jia-You; Liu, Yong; Xin, Wenjun

doi:10.1097/aln.0000000000001084

Cited by 42 publications

(41 citation statements)

References 43 publications

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“…33) Recently, evidence has emerged that the expression of TNF-α and IL-1β is increased in varieties of neuropathic pain models such as chronic sciatic nerve injury and oxaliplatin-induced peripheral neuropathic pain. [34][35][36] Peripheral or intrathecal application of TNF-α and IL-1β antagonists could effectively inhibit the pain. 37) Curcumin, as a phytochemical isolated from turmeric, has been investigated with promising anti-carcinogenic activity by in vitro and pre-clinical researches, and studies suggested that curcumin is able to target a range of tumorigenic pathways.…”

Section: Discussionmentioning

confidence: 99%

Curcumin Alleviates Oxaliplatin-Induced Peripheral Neuropathic Pain through Inhibiting Oxidative Stress-Mediated Activation of NF-κB and Mitigating Inflammation

Zhang

Guan

Wang

et al. 2020

Biological & Pharmaceutical Bulletin

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Oxaliplatin is a first-line clinical drug in cancer treatment and its side effects of peripheral neuropathic pain have also attracted much attention. Neuroinflammation induced by oxidative stress-mediated activation of nuclear factor-kappa B (NF-κB) plays an important role in the course. Current studies have shown that curcumin has various biological activities like antioxidant, anti-inflammatory, antitumor and so on, while few studies were conducted about its role in oxaliplatin-induced peripheral neuropathic pain. The aim of this study is to verify the mechanism of curcumin alleviating oxaliplatin-induced peripheral neuropathic pain. Intraperitoneal injection with oxaliplatin (4 mg/kg body weight) was given to the rats twice a week and last for four weeks to establish the model rats. Gavage administration of curcumin (12.5, 25, and 50 mg/kg body weight, respectively) was conducted for consecutive 28 d to explore the effects and potential mechanism. Our results showed that curcumin administration could increase mechanical withdrawal threshold and decrease the paw-withdrawal times of cold allodynia significantly; meanwhile, motor nerve conduction velocity (MNCV) and sense nerve conduction velocity (SNCV) were both increased and the injured neurons of the spinal cord were repaired. In addition, curcumin administration increased superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) and reduced malondialdehyde (MDA). Moreover, the curcumin operation inhibited the activated of NF-κB and level of inflammatory factors like tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6). In conclusion, these findings suggested that curcumin could alleviate oxaliplatin-induced peripheral neuropathic pain; the mechanism might be inhibiting oxidative stress-mediated activation of NF-κB and mitigating neuroinflammation.

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Section: Discussionmentioning

confidence: 99%

Curcumin Alleviates Oxaliplatin-Induced Peripheral Neuropathic Pain through Inhibiting Oxidative Stress-Mediated Activation of NF-κB and Mitigating Inflammation

Zhang

Guan

Wang

et al. 2020

Biological & Pharmaceutical Bulletin

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“…4,5 While CIN was described initially as a predominantly reversible condition that produced its effects within the peripheral nervous system, a growing body of evidence suggests that it persists long into survivorship 6 and that the neurotoxic effects can occur within the central nervous system. 7–9 Therefore, in this paper the abbreviation CIN was used instead of CIPN to describe this condition. Of note, in 2014, CIN was added to the National Comprehensive Cancer Center (NCCN) Clinical Practice Guideline for Survivorship 2,10 and the American Society of Clinical Oncology published a guideline on the prevention and management of CIN in cancer survivors.…”

Section: Introductionmentioning

confidence: 99%

Chemotherapy-Induced Neuropathy in Cancer Survivors

Miaskowski

Mastick

Paul

et al. 2017

Journal of Pain and Symptom Management

106

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Context Evidence suggests that chemotherapy-induced neuropathy (CIN) is a significant problem for cancer survivors. However, a detailed phenotypic characterization of CIN in cancer survivors is not available. Objectives To evaluate between group differences in demographic and clinical characteristics, as well as in measures of sensation, function, and postural control, in a sample of cancer survivors who received a platinum and/or a taxane-based CTX regimen and did (n=426) and did not (n=197) develop CIN. Methods Survivors completed self-report questionnaires and underwent objective testing (i.e., light touch, pain sensation, cold sensation, vibration, muscle strength, grip strength, Purdue Pegboard test, Timed Get Up and Go Test, Fullerton Advanced Balance test). Parametric and non-parametric statistics were used to compare between group differences in study outcomes. Results Of the 426 survivors with CIN, 4.9% had CIN only in their upper extremities, 27.0% only in their lower extremities, and 68.1% in both their upper and lower extremities. Demographic and clinical characteristics associated with CIN included: older age, lower annual income, higher body mass index, a higher level of comorbidity, being born prematurely, receipt of a higher cumulative dose of chemotherapy, and a poorer functional status. Survivors with CIN had worse outcomes for all of the following objective measures: light touch, pain, temperature, vibration, upper and lower extremity function and balance. Conclusions This study is the first to provide a detailed phenotypic characterization of CIN in cancer survivors who received a platinum and/or a taxane compound. These data can serve as a benchmark for future studies of CIN in cancer survivors.

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“… 6 , 7 Recently, CX3CL1 has been identified to mediate painful responses in chemotherapy drug-induced pain models. 8 – 10 Upregulation of CX3CL1 in spinal dorsal horn contributed to oxaliplatin-induced acute pain. 8 In addition, activation of CX3CL1/CX3CR1 signaling in DRG plays a pivotal role in paclitaxel-induced painful peripheral neuropathy.…”

Section: Introductionmentioning

confidence: 99%

Upregulation of CX3CL1 mediated by NF-κB activation in dorsal root ganglion contributes to peripheral sensitization and chronic pain induced by oxaliplatin administration

et al. 2017

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Painful peripheral neuropathy is a severe side effect in oxaliplatin therapy that compromises cancer patients' quality of life. However, its underlying pathogenic mechanisms remain largely unknown. Here, we found that intraperitoneal consecutive administration of oxaliplatin significantly increased excitability of small diameter dorsal root ganglion neurons and induced thermal hyperalgesia in rats. Furthermore, the CX3CL1 expression was significantly increased after oxaliplatin treatment, and intrathecal injection of a neutralizing antibody against CX3CL1 markedly attenuated the enhanced excitability of dorsal root ganglion neurons and thermal hyperalgesia. Importantly, the upregulated CX3CL1 is mediated by the NF-κB signaling pathway, as inhibition of NF-κB p65 activation with pyrrolidine dithiocarbamate or p65 siRNA inhibited the upregulation of CX3CL1, the enhanced excitability of dorsal root ganglion neurons, and thermal hyperalgesia induced by oxaliplatin. Further studies with chromatin immunoprecipitation found that oxaliplatin treatment increased the recruitment of NF-κB p65 to the CX3Cl1 promoter region. Our results suggest that upregulation of CX3CL1 in dorsal root ganglion mediated by NF-κB activation contributes to the peripheral sensitization and chronic pain induced by oxaliplatin administration.

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Cerebrospinal Fluid Oxaliplatin Contributes to the Acute Pain Induced by Systemic Administration of Oxaliplatin

Cited by 42 publications

References 43 publications

Curcumin Alleviates Oxaliplatin-Induced Peripheral Neuropathic Pain through Inhibiting Oxidative Stress-Mediated Activation of NF-κB and Mitigating Inflammation

Curcumin Alleviates Oxaliplatin-Induced Peripheral Neuropathic Pain through Inhibiting Oxidative Stress-Mediated Activation of NF-κB and Mitigating Inflammation

Chemotherapy-Induced Neuropathy in Cancer Survivors

Upregulation of CX3CL1 mediated by NF-κB activation in dorsal root ganglion contributes to peripheral sensitization and chronic pain induced by oxaliplatin administration

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