Huangqi Guizhi Wuwu Decoction can prevent and treat oxaliplatin-induced neuropathic pain by TNFα/IL-1β/IL-6/MAPK/NF-kB pathway

Li, Mingzhu; Li, Zheng; Ma, Xiande; Jin, Shengbo; Cao, Yang; Wang, Xuebing; Zhao, Jian; Wang, Jianbo; Wang, Xin; Xu, Jian

doi:10.18632/aging.203794

Cited by 17 publications

(10 citation statements)

References 28 publications

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“…[42] NF-κB p65 is translocated into the nucleus by activating p38 MAPK signaling, resulting in the development of NP. [43] In our study, the activation of p38 MAPK and NF-κB was observed in the spinal dorsal horn of CCI-treated rats, in line with Dai's research. [44] Following the administration of the GPR39 agonist, the p38 MAPK/NF-κB signaling was markedly repressed, implying that the impact of the GPR39 agonist on the activation of microglia in CCI-treated rats might be regulated by suppressing the p38 MAPK/NF-κB signaling pathway.…”

Section: Discussionsupporting

confidence: 89%

Activation of G protein‐coupled receptor 39 alleviates neuropathic pain and chronic inflammation

Cheng,

Yan,

Yang

et al. 2023

J Biochem & Molecular Tox

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Neuropathic pain (NP) is mainly caused by lesions or diseases of the somatosensory nervous system and triggers severe physical burdens to patients. It is claimed that activated microglia‐mediated neuroinflammation participates in the development of NP, which is regulated by p38 mitogen‐activated protein kinase (MAPK)/nuclear factor‐κappa B (NF‐κB) p65 signaling. G protein‐coupled receptor 39 (GPR39) is a trans‐membrane protein involved in the activation of cellular transduction pathways, and TC‐G 1008, a GPR39 agonist, is believed to have inhibitory effects on neuroinflammation. Our study will explore the possible alleviatory function of TC‐G 1008 on NP in a rat model. GPR39 was found markedly downregulated in the spinal dorsal horn of chronic constriction injury (CCI)‐stimulated rats. Rats were treated with CCI, followed by intranasal administration with 7.5 and 15 mg/kg TC‐G 1008 at 1, 25, 49, and 73 h postmodeling, respectively. Drastically lowered values of paw withdrawal threshold and paw withdrawal latency, upregulated ionized calcium‐binding adapter molecule 1, increased release of inflammatory cytokines, elevated spinal malondialdehyde levels, and reduced spinal glutathione peroxidase levels were observed in CCI‐stimulated rats, all of which were markedly alleviated and rescued by TC‐G 1008. Furthermore, the levels of p‐p38/p38 and p‑NF‑κB p65 were found signally repressed in the spinal dorsal horn of CCI‐stimulated rats, which was notably reversed by TC‐G 1008. Collectively, TC‐G 1008 markedly alleviated NP and neuroinflammation in CCI‐treated rats. Our findings provide an attractive future direction for the treatment of NP.

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Section: Discussionsupporting

confidence: 89%

Activation of G protein‐coupled receptor 39 alleviates neuropathic pain and chronic inflammation

Cheng,

Yan,

Yang

et al. 2023

J Biochem & Molecular Tox

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“…Traditional Chinese medicine categorizes DVT as “pulse obstruction” and “blood stasis.” [ 11 ] Sun Simiao, a renowned Chinese physician over a thousand years ago, noted in Qian Jin Bei Ji Yao Fang that poor blood circulation is the root cause of thrombosis: “if qi and blood are stagnant, there will be pain; if the pulse is blocked, there will be swelling, and if stagnation persists for a long time, heat will arise.” HQGZWWD is composed of five traditional Chinese medicines: Huangqi ( Hedysarum multijugum maxim , HM), Guizhi ( Cinnamomi Ramulus , CR), Baishao ( Paeoniae Radix Alba , PA), Shengjiang ( Zingiber officinale Roscoe , ZR), and Dazao (Jujubae Fructus , JF) [ 12 ]. HQGZWWD is a medicinal formula that promotes blood circulation and nourishes the qi; this was reported by Zhang Zhongjing, a medical expert from the Eastern Han Dynasty (approximately 154–219 AD), in his book “Jin Gui Yao Lue” almost 2000 years ago [ 13 ]. Additionally, various medical books such as “San Yin Ji Yi Bing Zheng Fang Lun” from the Southern Song Dynasty (1174 AD), “Zheng Zhi Zhun Sheng: Lei Fang” from the Ming Dynasty (1602 AD) and “Yi Fang Ji Jie” from the Qing Dynasty recorded the effectiveness of HQGZWWD in treating DVT.…”

Section: Introductionmentioning

confidence: 99%

Network pharmacology prediction and molecular docking-based strategy to discover the potential pharmacological mechanism of Huang–Qi–Gui–Zhi–Wu–Wu decoction against deep vein thrombosis

et al. 2023

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Background Huangqi Guizhi Wuwu decoction (HQGZWWD) has been used to treat and prevent deep vein thrombosis (DVT) in China. However, its potential mechanisms of action remain unclear. This study aimed to utilize network pharmacology and molecular docking technology to elucidate the molecular mechanisms of action of HQGZWWD in DVT. Methods We identified the main chemical components of HQGZWWD by reviewing the literature and using a Traditional Chinese Medicine Systems Pharmacology (TCMSP) database. We used GeneCards and Online Mendelian Inheritance in Man databases to identify the targets of DVT. Herb-disease-gene-target networks using Cytascape 3.8.2 software; a protein–protein interaction (PPI) network was constructed by combining drug and disease targets on the STRING platform. Additionally, we conducted Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. Finally, molecular docking verification of active components and core protein targets was conducted. Results A total of 64 potential targets related to DVT were identified in HQGZWWD, with 41 active components; quercetin, kaempferol, and beta-sitosterol were the most effective compounds. The PPI network analysis revealed that AKT1, IL1B, and IL6 were the most abundant proteins with the highest degree. GO analysis indicated that DVT treatment with HQGZWWD could involve the response to inorganic substances, positive regulation of phosphorylation, plasma membrane protein complexes, and signaling receptor regulator activity. KEGG analysis revealed that the signaling pathways included pathways in cancer, lipid and atherosclerosis, fluid shear stress and atherosclerosis, and the phosphatidylinositol 3-kinases/protein kinase B(PI3K-Akt) and mitogen-activated protein kinase (MAPK) signaling pathways. The molecular docking results indicated that quercetin, kaempferol, and beta-sitosterol exhibited strong binding affinities for AKT1, IL1B, and IL6. Conclusion Our study suggests that AKT1, IL1B, and IL6 are promising targets for treating DVT with HQGZWWD. The active components of HQGZWWD likely responsible for its effectiveness against DVT are quercetin, kaempferol, and beta-sitosterol, they may inhibit platelet activation and endothelial cell apoptosis by regulating the PI3K/Akt and MAPK signaling pathways, slowing the progression of DVT.

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“…138 Oxaliplatin is one of the cancer-related drugs used in treating colon and rectal cancer that can lead to neuropathic pain. 139 The main mechanism of neuropathic pain is under debate. In vivo studies have suggested several mechanisms for neuropathic pain, but these mechanisms in humans may differ completely.…”

Section: The Role Of Micrornas In Oxaliplatin-induced Neuropathic Painmentioning

confidence: 99%

The Role of microRNAs in Regulating Cancer Cell Response to Oxaliplatin-Containing Regimens

Tavakoli Pirzaman,

Ebrahimzadeh Pirshahid,

Babajani

et al. 2023

Technol Cancer Res Treat

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Oxaliplatin (cyclohexane-1,2-diamine; oxalate; platinum [2+]) is a third-generation chemotherapeutic drug with anticancer effects. Oxaliplatin has a role in the treatment of several cancers. It is one of the few drugs which can eliminate the neoplastic cells of colorectal cancer. Also, it has an influential role in breast cancer, lung cancer, bladder cancer, prostate cancer, and gastric cancer. Although oxaliplatin has many beneficial effects in cancer treatment, resistance to this drug is in the way to cure neoplastic cells and reduce treatment efficacy. microRNAs are a subtype of small noncoding RNAs with ∼22 nucleotides that exist among species. They have diverse roles in physiological processes, including cellular proliferation and cell death. Moreover, miRNAs have essential roles in resistance to cancer treatment and can strengthen sensitivity to chemotherapeutic drugs and regimens. In colorectal cancer, the co-treatment of oxaliplatin with anti-miR-19a can partially reverse the oxaliplatin resistance through the upregulation of phosphatase and tensin homolog (PTEN). Moreover, by preventing the spread of gastric cancer cells and downregulating glypican-3 (GPC3), MiR-4510 may modify immunosuppressive signals in the tumor microenvironment. Treatment with oxaliplatin may develop into a specialized therapeutic drug for patients with miR-4510 inhibition and glypican-3-expressing gastric cancer. Eventually, miR-122 upregulation or Wnt/β-catenin signaling suppression boosted the death of HCC cells and made them more sensitive to oxaliplatin. Herein, we have reviewed the role of microRNAs in regulating cancer cells’ response to oxaliplatin, with particular attention to gastrointestinal cancers. We also discussed the role of these noncoding RNAs in the pathophysiology of oxaliplatin-induced neuropathic pain.

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Huangqi Guizhi Wuwu Decoction can prevent and treat oxaliplatin-induced neuropathic pain by TNFα/IL-1β/IL-6/MAPK/NF-kB pathway

Cited by 17 publications

References 28 publications

Activation of G protein‐coupled receptor 39 alleviates neuropathic pain and chronic inflammation

Activation of G protein‐coupled receptor 39 alleviates neuropathic pain and chronic inflammation

Network pharmacology prediction and molecular docking-based strategy to discover the potential pharmacological mechanism of Huang–Qi–Gui–Zhi–Wu–Wu decoction against deep vein thrombosis

The Role of microRNAs in Regulating Cancer Cell Response to Oxaliplatin-Containing Regimens

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