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Clinical Efficacy of Ultrasonic Medicinal Penetration in the Removal of Blood Stasis and Alleviation of Zhuyu Juanbi Formula in the Treatment of Peripheral Neuropathy Induced by Paclitaxel
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作者 Ying Zhang Huixin Chen +2 位作者 Qirong Zhang Yingjie Jia Dan Yi 《Proceedings of Anticancer Research》 2024年第3期7-17,共11页
Objective: To observe the clinical efficacy and differences of the Zhuyu Juanbi formula delivered through ultrasound at Zusanli on patients with chemotherapy-induced peripheral neuropathy (CIPN) due to paclitaxel inje... Objective: To observe the clinical efficacy and differences of the Zhuyu Juanbi formula delivered through ultrasound at Zusanli on patients with chemotherapy-induced peripheral neuropathy (CIPN) due to paclitaxel injection. Methods: A total of 72 breast cancer patients with CIPN were randomly divided into two groups. The treatment group (36 cases) was treated with oral methylcobalamin plus ultrasonic medicine permeating Zhuyu Juanbi formulae, while the control group (36 cases) was treated with oral methylcobalamin alone. Following two 2 cycles of continuous treatment, the efficacy of peripheral neurotoxicity, TCM syndrome score, FACT/GOG-Ntx score, total neuropathy score, and safety indicators of gynecological cancer patients were observed in the two groups. Result: In the treatment of CIPN, the addition of ultrasonic medicine permeating Zhuyu Juanbi formulae was more effective than oral methylcobalamin alone in reducing peripheral neurotoxicity and improving the quality of life of patients. The difference between the two groups was statistically significant (P < 0.05), and ultrasound drug penetration Zhuyu Juanbi formulae significantly reduced the FACT/ GOG-Ntx score and TNS score in the treatment group. In terms of drug safety, it rarely caused adverse reactions such as grade 3 and 4 leukopenia, and the safety profile was therefore good. Conclusion: The combination of ultrasonic medicine permeating Zhuyu Juanbi formulae and methylcobalamin has been demonstrated to be an effective treatment for peripheral neurotoxicity in patients with PIPN. It has been shown to significantly improve the clinical symptoms of PIPN patients, improve the quality of life of patients, and have a good safety profile. 展开更多
关键词 Chemotherapy-induced peripheral neuropathy(CIPN) paclitaxel-induced peripheral neuropathy Zhuyu Juanbi formulae Ultrasonic drug delivery
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Antinociceptive activity of transient receptor potential channel TRPV1, TRPA1, and TRPM8 antagonists in neurogenic and neuropathic pain models in mice 被引量:5
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作者 Kinga SALAT Barbara FILIPEK 《Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)》 SCIE CAS CSCD 2015年第3期167-178,共12页
The aim of this research was to assess the antinociceptive activity of the transient receptor potential (TRP) channel TRPV1, TRPM8, and TRPA1 antagonists in neurogenic, tonic, and neuropathic pain models in mice. Fo... The aim of this research was to assess the antinociceptive activity of the transient receptor potential (TRP) channel TRPV1, TRPM8, and TRPA1 antagonists in neurogenic, tonic, and neuropathic pain models in mice. For this purpose, TRP channel antagonists were administered into the dorsal surface of a hind paw 15 min before capsaicin, allyl isothiocyanate (AITC), or formalin. Their antiallodynic and antihyperalgesic efficacies after intraperitoneal ad- ministration were also assessed in a paclitaxel-induced neuropathic pain model. Motor coordination of paclitaxel- treated mice that received these TRP channel antagonists was investigated using the rotarod test. TRPV1 antagonists, capsazepine and SB-366791, attenuated capsaicin-induced nociceptive reaction in a concentration-dependent manner. At 8 pg/20 pl, this effect was 51% (P〈0.001) for capsazepine and 37% (P〈0.05) for SB-366791. A TRPA1 antagonist, A-967079, reduced pain reaction by 48% (P〈0.05) in the AITC test and by 54% (P〈0.001) in the early phase of the formalin test. The test compounds had no influence on the late phase of the formalin test. In paclitaxel-treated mice, they did not attenuate heat hyperalgesia but N-(3-aminopropyl)-2-{[(3-methylphenyl)methyl]oxy}-N-(2-thienylmethyl) benzamide hydrochloride salt (AMTB), a TRPM8 antagonist, reduced cold hyperalgesia and tactile allodynia by 31% (P〈0.05) and 51% (P〈0.01), respectively. HC-030031, a TRPA1 channel antagonist, attenuated tactile allodynia in the von Frey test (62%; P〈0.001). In conclusion, distinct members of TRP channel family are involved in different pain models in mice. Antagonists of TRP channels attenuate nocifensive responses of neurogenic, tonic, and neuropathic pain, but their efficacies strongly depend on the pain model used. 展开更多
关键词 Allyl isothiocyanate CAPSAICIN FORMALIN Neurogenic pain Transient receptor potential channels paclitaxel-induced sensory neuropathy
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基于网络药理学的补阳还五汤治疗紫杉醇导致的周围神经病变的作用机制
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作者 任丽琦 孙涛 徐君南 《中国医药指南》 2023年第13期120-122,126,共4页
目的利用网络药理学技术研究补阳还五汤用于治疗紫杉醇导致的周围神经病变(PIPN)的作用机制。方法通过TCMSP平台以及相关文献筛选补阳还五汤组方主要活性成分及其对应靶点,构建药物疾病交集靶点,通过Cytoscape筛选核心化合物和核心靶点... 目的利用网络药理学技术研究补阳还五汤用于治疗紫杉醇导致的周围神经病变(PIPN)的作用机制。方法通过TCMSP平台以及相关文献筛选补阳还五汤组方主要活性成分及其对应靶点,构建药物疾病交集靶点,通过Cytoscape筛选核心化合物和核心靶点绘制关系网络。结果经分析获得104个活性成分和与PIPN的共同靶点97个,补阳还五汤治疗PIPN主要涉及Wnt及STAT3等信号通路,通槲皮素、木犀草素等潜在核心成分,作用于AKT1、CASP3、CDKN1A等潜在核心靶点。结论本研究探究了补阳还五汤治疗PIPN的作用机制可能与ErbB及EGFR等信号通路相关。 展开更多
关键词 紫杉醇导致的周围神经病变 PIPN 补阳还五汤 网络药理学 EGFR
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电针足三里对紫杉醇诱导神经性疼痛小鼠脾脏及脊髓背角α7nAChR调控炎症的机制研究 被引量:3
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作者 庞莉娜 兰艳艳 +2 位作者 王志福 陈小梅 俞向梅 《康复学报》 CSCD 2022年第5期426-433,共8页
目的:探讨电针足三里对化疗药物紫杉醇诱导神经性疼痛(PINP)小鼠脾脏及脊髓背角α7烟碱型乙酰胆碱受体(α7nAChR)影响炎症变化的作用机制。方法:选择雄性成年C57BL/6小鼠60只,体质量18~22 g,按照随机数字表法分为对照组、模型组、电针... 目的:探讨电针足三里对化疗药物紫杉醇诱导神经性疼痛(PINP)小鼠脾脏及脊髓背角α7烟碱型乙酰胆碱受体(α7nAChR)影响炎症变化的作用机制。方法:选择雄性成年C57BL/6小鼠60只,体质量18~22 g,按照随机数字表法分为对照组、模型组、电针组、腹腔拮抗剂组、鞘内拮抗剂组,每组12只。模型组、电针组、腹腔拮抗剂组和鞘内拮抗剂组腹腔隔日注射紫杉醇(2 mg/kg),总计4次,建立PINP模型,对照组给予同等容量的生理盐水。电针组、腹腔拮抗剂组、鞘内拮抗剂组从造模第1天开始进行电针干预,隔日1次,共干预7次。腹腔拮抗剂组、鞘内拮抗剂组分别于造模第1、7、13天分别在腹腔、鞘内注射α7nAChR拮抗剂α-银环蛇毒素(α-BGT)。采用Von Frey测痛仪及热刺痛仪检测造模第0、7、14天小鼠机械痛阈值(PWT)及热痛阈值(PWL)的变化;采用Western blot检测造模第14天小鼠脾脏、脊髓背角α7nAChR蛋白表达;采用RT-qPCR及ELISA法检测造模第14天小鼠脾脏、脊髓背角TNF-αmRNA水平及蛋白表达的变化。结果:(1)行为学测试:5组小鼠造模前PWT和PWL比较,差异无统计学意义(P>0.05);模型组造模第7、14天PWT和PWL较同时段对照组小鼠显著下降,差异有统计学意义(P<0.05);电针组造模第7、14天PWT和PWL较同时段模型组小鼠明显上升,差异有统计学意义(P<0.05);腹腔拮抗剂组、鞘内拮抗剂组小鼠造模第7、14天PWT和PWL较同时段电针组小鼠显著下降,差异有统计学意义(P<0.05)。(2) α7nAChR蛋白表达测试:与对照组比较,模型组小鼠脾脏及脊髓背角α7nAChR蛋白表达显著降低,差异有统计学意义(P<0.05);与模型组比较,电针组小鼠脾脏及脊髓背角α7nAChR蛋白表达显著升高,差异有统计学意义(P<0.05)。(3)TNF-αmRNA水平及蛋白表达测试:与对照组比较,模型组小鼠脾脏、脊髓背角TNF-αmRNA水平及蛋白表达显著升高,差异有统计学意义(P<0.05);与模型组比较 展开更多
关键词 紫杉醇诱导神经性疼痛 电针 足三里 脾脏 脊髓背角 α7nAChR
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压迫疗法对紫杉醇致周围神经病变的效果
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作者 何慧敏 钟雅芳 +1 位作者 薛晓琳 张宏 《当代医学》 2023年第24期171-174,共4页
目的探讨压迫疗法对预防紫杉醇致周围神经病变(PIPN)的效果。方法选取2018年5月至2020年4月福建省肿瘤医院收治的130例肺癌化疗患者作为研究对象,采用随机数字表法分为实验组(n=61)与对照组(n=62)。对照组采用常规护理措施,实验组在对... 目的探讨压迫疗法对预防紫杉醇致周围神经病变(PIPN)的效果。方法选取2018年5月至2020年4月福建省肿瘤医院收治的130例肺癌化疗患者作为研究对象,采用随机数字表法分为实验组(n=61)与对照组(n=62)。对照组采用常规护理措施,实验组在对照组护理基础上佩戴外科手套和弹力袜进行压迫疗法。比较两组PIPN严重程度及手背温度。结果实验组紫杉醇剂量改变占比为19.7%,低于对照组的38.7%,差异有统计学意义(P<0.05)。第2次、第4次化疗及化疗后3个月,实验组PIPN严重程度均低于对照组,差异有统计学意义(P<0.05)。第2次、第4次化疗佩戴手套前,两组右手手背温度比较差异无统计学意义;摘除手套后,实验组手背温度低于佩戴手套前和对照组,差异有统计学意义(P<0.05)。结论压迫疗法具有安全、耐受性好的特点,可降低PIPN的发生率,有利于肺癌患者完成化疗计划。 展开更多
关键词 压迫疗法 紫杉醇致周围神经病变 肺癌 生命质量
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吡格列酮影响紫杉醇诱导神经痛大鼠的作用机制
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作者 张月荣 张丽萍 +2 位作者 章阳 贾宏彬 陈珍珍 《医学研究与战创伤救治》 CAS 北大核心 2023年第5期463-467,共5页
目的研究吡格列酮对紫杉醇诱导神经痛大鼠的影响及其机制探讨。方法随机区组设计将32只雄性大鼠分为4组:空白组、安慰剂组、吡格列酮治疗组和吡格列酮拮抗剂(GW9662)组,每组8只。空白组大鼠在第1、3、5、7天,腹腔注射等渗盐水(1 mL/kg)... 目的研究吡格列酮对紫杉醇诱导神经痛大鼠的影响及其机制探讨。方法随机区组设计将32只雄性大鼠分为4组:空白组、安慰剂组、吡格列酮治疗组和吡格列酮拮抗剂(GW9662)组,每组8只。空白组大鼠在第1、3、5、7天,腹腔注射等渗盐水(1 mL/kg),其余组大鼠腹腔注射紫杉醇(2 mg/kg)制备紫杉醇诱导的慢性神经病理性疼痛大鼠模型。第7天测定大鼠冷缩足反应阈值(TNCW)后,吡格列酮治疗组大鼠腹腔注射吡格列酮(10 mg/kg),连续7 d;拮抗剂组大鼠在吡格列酮给药前30 min腹腔注射GW9662(2 mg/kg);安慰剂组腹腔连续7 d注射赋形剂(2 mL/kg)。所有大鼠于干预前、干预后第1、3、5、7、9、11、13、14天测定冷缩足反应阈值;第14天检测腰脊髓细胞因子TNF-α、IL-1β和脊髓胶质细胞酸性蛋白(GFAP)mRNA表达水平。结果与空白组相比,腹腔注射紫杉醇各组大鼠TNCW次数明显增加(P<0.05),成模各组大鼠脊髓L5脊髓中TNF-α和IL-1β表达明显增高(P<0.05);与安慰剂组比,在注射吡格列酮后治疗组大鼠TNCW次数显著下降(P<0.05),治疗组L5脊髓组织中TNF-α、IL-1β水平明显下降(P<0.05);拮抗剂组与安慰剂组比差异均无统计学意义(P>0.05)。与空白组大鼠L5脊髓腰胶质细胞表面标志物GFAP的mRNA表达水平(92.88±8.15)相比,安慰剂组、治疗组、拮抗剂组(258.63±9.41,191.25±6.45,251.25±4.13)明显升高(P<0.05);与安慰剂组相比,治疗组GFAP mRNA表达水平显著下降(P<0.05),而拮抗剂组差异无统计学意义(P>0.05)。结论吡格列酮抑制了脊髓星形胶质细胞活性和TNF-α、IL-1β的表达、改善紫杉醇诱导的大鼠冷痛觉过敏,可能与PPARγ活性增加有关。 展开更多
关键词 紫杉醇诱导神经病理性疼痛 PPARΓ 痛觉过敏 胶质细胞 炎症细胞因子
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