Abstract
Chemotherapy-induced peripheral neuropathy (CIPN) is a dose-limiting side effect caused by chemotherapy drugs, and its existence seriously affects the quality of life of patients. We first established an oxaliplatin-induced peripheral neuropathy (OIPN) model and then measured and evaluated mechanical hyperalgesia, thermal nociception, cold allodynia, and intraepidermal nerve fiber (IENF) density to determine Siwei Jianbu Decoction's role in preventing OIPN. Then, we conducted a systematic pharmacological study that revealed important roles for the MAPK signaling pathway and proinflammatory immune pathway and confirmed these roles by western blot, immunofluorescence, and qPCR. The data show that Siwei Jianbu Decoction can effectively prevent oxaliplatin-induced neuroinflammation by inhibiting an increase in NF-κB expression via downregulation of p-ERK1/2 and p-p38. The present study showed that SWJB may be beneficial in preventing oxaliplatin-induced peripheral neuropathy.
Highlights
Colorectal cancer has become a common type of cancer, and its present global incidence and mortality rate are among the highest
It has been shown that the activation of glial cells and the upregulation of proinflammatory cytokines play a crucial role in the occurrence and development of chemotherapy-induced neuropathic pain [5]
We found that inflammation may be related to nuclear factor kappa-B (NF-κB) and extracellular regulated protein kinases (ERK/p38) mitogen-activated protein kinase (MAPK) signaling pathways in mouse models of oxaliplatin-induced peripheral neuropathic pain (OIPN)
Summary
Colorectal cancer has become a common type of cancer, and its present global incidence and mortality rate are among the highest. Hyperalgesia, dysesthesia, and paranaesthesia [4]. These side effects limit the use of oxaliplatin. We know that the MAPK signaling system is activated by extracellular stimuli, leading to an intracellular response. These stimuli provide links between transmembrane signal transduction and transcriptional changes in different environmental signals, such as cytokines, growth factors, oxidative stress, and inflammation [8]. We found that inflammation may be related to nuclear factor kappa-B (NF-κB) and extracellular regulated protein kinases (ERK/p38) MAPK signaling pathways in mouse models of oxaliplatin-induced peripheral neuropathic pain (OIPN). Studies have found that celecoxib reduces oxaliplatin-induced hyperalgesia by inhibiting ERK1/2 signaling in the spinal cord [9], and the major drugs used clinically for the prevention and treatment of OIPN, such as glutathione, vitamin E, amifolin, amantadine, mannitrite, and norepinephrine reuptake inhibitors, are not effective against neuroinflammation in OIPN [10, 11]
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