目的:观察芩夏清热祛风颗粒对感染后咳嗽(PIC)模型大鼠血清P物质(SP)、神经激肽A (NKA)、神经激肽B (NKB)、降钙素基因相关肽(CGRP)含量及肺组织SP、NKA、NKB、CGRP蛋白表达水平的影响,探讨芩夏清热祛风颗粒改善PIC气道神经源性炎症的...目的:观察芩夏清热祛风颗粒对感染后咳嗽(PIC)模型大鼠血清P物质(SP)、神经激肽A (NKA)、神经激肽B (NKB)、降钙素基因相关肽(CGRP)含量及肺组织SP、NKA、NKB、CGRP蛋白表达水平的影响,探讨芩夏清热祛风颗粒改善PIC气道神经源性炎症的作用机制。方法:将60只SPF级SD雄性大鼠按照随机数字表法分为空白组、模型组、对照组和低、中、高剂量组各10只。空白组不予造模,其余各组均采用烟熏结合脂多糖(LPS)溶液滴鼻及辣椒素雾化吸入制备感染后咳嗽大鼠模型。造模成功后,对照组按体质量4.78 ml/(kg∙d)给予复方甲氧那明溶液灌胃,低、中、高剂量组分别按体质量44.2 ml/(kg∙d)、93.6 ml/(kg∙d)、127.8 ml/(kg∙d)给予芩夏清热祛风颗粒溶液灌胃,空白组、模型组按体质量10 mL/(kg∙d) 0.9% NaCl灌胃给药,每天1次,连续14 d,空白组不做任何处理。观察6组大鼠末次给药后3min内咳嗽次数,HE染色观察6组大鼠肺组织病理形态学变化,ELISA法检测6组大鼠血清SP、NKA、NKB、CGRP含量,免疫组化法检测6组大鼠肺组织SP、NKA、NKB、CGRP蛋白表达。结果:与空白组比较,模型组末次给药后3min咳嗽次数明显增多(P 0.05);与对照组比较,中、高剂量组血清SP、NKA、NKB、CGRP含量和肺组织SP、NKA、NKB、CGRP蛋白表达水平无显著性差异(P > 0.05),低剂量组血清SP、NKA、NKB、CGRP含量和肺组织SP、NKA、NKB、CGRP蛋白表达水平较高(P Objective: To observe the effects of Qinxia Qingre Qufeng Granules on the levels of serum substance P (SP), neurokinin A (NKA), neurokinin B (NKB), and calcitonin gene-related peptide (CGRP) and the expression levels of SP, NKA, NKB, and CGRP proteins in lung tissues in rats with post-infectious cough (PIC) model, and to explore the mechanism of action of Qinxia Qingre Qufeng Granules in improving airway neurogenic inflammation in PIC. Methods: Sixty SPF SD male rats were randomly divided into blank group, model group, control group, and low, medium, and high dose groups, with 10 rats in each group. No model was established in the blank group, and the rat model of post-infectious cough was established in the other groups by smoke combined with lipopolysaccharide (LPS) solution nasal drops and capsaicin atomization inhalation. After successful modeling, the control group was given compound methoxyphenamine solution by gavage at 4.78 ml/(kg·d) of body weight, the low, medium and high dose groups were given Qinxia Qingre Qufeng granule solution by gavage at 44.2 ml/(kg·d), 93.6 ml/(kg·d) and 127.8 ml/(kg·d) of body weight, respectively, the blank group and model group were given 0.9% NaCl by gavage at 10 mL/(kg·d) of body weight, once a day for 14 consecutive days, and the blank group did not receive any treatment. The number of coughs within 3 minutes after the last administration was observed in the six groups of rats, the pathological morphological changes of the lung tissues of the six groups of rats were observed by HE staining, the serum SP, NKA, NKB and CGRP levels of the six groups of rats were detected by ELISA, and the SP, NKA, NKB and CGRP protein expressions of the lung tissues of the six groups of rats were detected by immunohistochemistry. Results: Compared with the blank group, the number of coughs in the model group increased significantly 3 minutes after the last administration (P 0.05). Compared with the control group, there were no significant differences in the serum SP, NKA, NKB, and CGRP levels and the protein expression levels of SP, NKA, NKB, and CGRP in lung tissues of the medium- and high-dose groups (P > 0.05), and the serum SP, NKA, NKB, and CGRP levels and the protein expression levels of SP, NKA, NKB, and CGRP in lung tissues of the low-dose group were higher (P < 0.05). Conclusion: Qinxia Qingre Qufeng Granule can reduce the serum SP, NKA, NKB, and CGRP levels of PIC rats, inhibit the protein expression of SP, NKA, NKB, and CGRP in rat lung tissues, and reduce the inflammatory infiltration of lung tissues, thereby reducing airway neurogenic inflammation and promoting disease recovery.展开更多
背景:运动干预作为经济有效的非物理疗法,可有效上调脑源性神经营养因子表达进而防治帕金森病发生发展,但目前关于靶向脑源性神经营养因子的运动治疗策略在延缓帕金森病发生发展的潜在作用机制尚不明晰。目的:以脑源性神经营养因子和帕...背景:运动干预作为经济有效的非物理疗法,可有效上调脑源性神经营养因子表达进而防治帕金森病发生发展,但目前关于靶向脑源性神经营养因子的运动治疗策略在延缓帕金森病发生发展的潜在作用机制尚不明晰。目的:以脑源性神经营养因子和帕金森病的关系为切入点,分析帕金森病病理状态下运动对脑源性神经营养因子表达的特异性调控作用及机制,梳理脑源性神经营养因子介导下不同运动方式对帕金森病的改善效果,并阐明靶向脑源性神经营养因子的运动治疗策略在防治帕金森病的潜在作用机制,旨在为运动防治帕金森病提供新的理论依据。方法:以“帕金森病,脑源性神经营养因子,神经保护,多巴胺,神经元异常凋亡,神经炎症反应,突触可塑性,运动”等为中文检索词;以“Parkinson’s disease,BDNF,Neuroprotection,neuroinflammation,synaptic plasticity”等为英文检索词,分别检索中国知网、万方数据库、PubMed和Web of Science数据库,搜寻各数据库建库至2024年2月发表的所有研究文献,根据纳排标准共获得核心相关文献98篇。结果与结论:①在帕金森病理背景下,运动可通过促进肌因子鸢尾素大量分泌,并降低色氨酸-犬尿氨酸代谢途径紊乱特异性调控脑源性神经营养因子表达。②有氧运动,尤其是特殊有氧运动(动物:旋转杆步行/人类:北欧健走)以及多模式运动可显著上调脑源性神经营养因子表达,进而改善帕金森病的运动症状,此外脑源性神经营养因子还介导身心运动(太极拳)对帕金森病患者认知障碍和睡眠障碍等非运动症状的有效调节。③运动诱导的高表达脑源性神经营养因子可能通过上调抗炎因子白细胞介素10、神经生长因子β和转化生长因子β表达,下调促炎因子肿瘤坏死因子α及白细胞介素1β表达,并抑制核转录因子κB信号通路表达降低小胶质细胞活性减轻神经炎症反应;增加酪氨酸羟化酶活性以促进多巴胺合成释放,并通过下调基质金属蛋白酶3及糖原合成酶激酶3β表达抑制α-突触核蛋白在丝氨酸129位点的磷酸化修饰,以防止神经异常凋亡;诱导突触效能的长时程增强发生,促进突触后致密区蛋白95及突触素大量表达以改善突触可塑性,发挥神经保护作。④鉴于脑源性神经营养因子在帕金森病发病进程及治疗中发挥重要作用,靶向脑源性神经营养因子的运动治疗策略将有助于推动帕金森病疾病“运动+药物”精准医疗的发展。但由于目前研究采用的运动处方较为单一,且研究焦点主要围绕运动症状而缺乏对非运动症状的考察,因此亟待学者采用更加统一和系统的运动处方,围绕非有氧运动类型对同一批帕金森病患者进行长期纵向跟踪研究,以此完善帕金森病运动防治领域研究的不足。展开更多
文摘目的:观察芩夏清热祛风颗粒对感染后咳嗽(PIC)模型大鼠血清P物质(SP)、神经激肽A (NKA)、神经激肽B (NKB)、降钙素基因相关肽(CGRP)含量及肺组织SP、NKA、NKB、CGRP蛋白表达水平的影响,探讨芩夏清热祛风颗粒改善PIC气道神经源性炎症的作用机制。方法:将60只SPF级SD雄性大鼠按照随机数字表法分为空白组、模型组、对照组和低、中、高剂量组各10只。空白组不予造模,其余各组均采用烟熏结合脂多糖(LPS)溶液滴鼻及辣椒素雾化吸入制备感染后咳嗽大鼠模型。造模成功后,对照组按体质量4.78 ml/(kg∙d)给予复方甲氧那明溶液灌胃,低、中、高剂量组分别按体质量44.2 ml/(kg∙d)、93.6 ml/(kg∙d)、127.8 ml/(kg∙d)给予芩夏清热祛风颗粒溶液灌胃,空白组、模型组按体质量10 mL/(kg∙d) 0.9% NaCl灌胃给药,每天1次,连续14 d,空白组不做任何处理。观察6组大鼠末次给药后3min内咳嗽次数,HE染色观察6组大鼠肺组织病理形态学变化,ELISA法检测6组大鼠血清SP、NKA、NKB、CGRP含量,免疫组化法检测6组大鼠肺组织SP、NKA、NKB、CGRP蛋白表达。结果:与空白组比较,模型组末次给药后3min咳嗽次数明显增多(P 0.05);与对照组比较,中、高剂量组血清SP、NKA、NKB、CGRP含量和肺组织SP、NKA、NKB、CGRP蛋白表达水平无显著性差异(P > 0.05),低剂量组血清SP、NKA、NKB、CGRP含量和肺组织SP、NKA、NKB、CGRP蛋白表达水平较高(P Objective: To observe the effects of Qinxia Qingre Qufeng Granules on the levels of serum substance P (SP), neurokinin A (NKA), neurokinin B (NKB), and calcitonin gene-related peptide (CGRP) and the expression levels of SP, NKA, NKB, and CGRP proteins in lung tissues in rats with post-infectious cough (PIC) model, and to explore the mechanism of action of Qinxia Qingre Qufeng Granules in improving airway neurogenic inflammation in PIC. Methods: Sixty SPF SD male rats were randomly divided into blank group, model group, control group, and low, medium, and high dose groups, with 10 rats in each group. No model was established in the blank group, and the rat model of post-infectious cough was established in the other groups by smoke combined with lipopolysaccharide (LPS) solution nasal drops and capsaicin atomization inhalation. After successful modeling, the control group was given compound methoxyphenamine solution by gavage at 4.78 ml/(kg·d) of body weight, the low, medium and high dose groups were given Qinxia Qingre Qufeng granule solution by gavage at 44.2 ml/(kg·d), 93.6 ml/(kg·d) and 127.8 ml/(kg·d) of body weight, respectively, the blank group and model group were given 0.9% NaCl by gavage at 10 mL/(kg·d) of body weight, once a day for 14 consecutive days, and the blank group did not receive any treatment. The number of coughs within 3 minutes after the last administration was observed in the six groups of rats, the pathological morphological changes of the lung tissues of the six groups of rats were observed by HE staining, the serum SP, NKA, NKB and CGRP levels of the six groups of rats were detected by ELISA, and the SP, NKA, NKB and CGRP protein expressions of the lung tissues of the six groups of rats were detected by immunohistochemistry. Results: Compared with the blank group, the number of coughs in the model group increased significantly 3 minutes after the last administration (P 0.05). Compared with the control group, there were no significant differences in the serum SP, NKA, NKB, and CGRP levels and the protein expression levels of SP, NKA, NKB, and CGRP in lung tissues of the medium- and high-dose groups (P > 0.05), and the serum SP, NKA, NKB, and CGRP levels and the protein expression levels of SP, NKA, NKB, and CGRP in lung tissues of the low-dose group were higher (P < 0.05). Conclusion: Qinxia Qingre Qufeng Granule can reduce the serum SP, NKA, NKB, and CGRP levels of PIC rats, inhibit the protein expression of SP, NKA, NKB, and CGRP in rat lung tissues, and reduce the inflammatory infiltration of lung tissues, thereby reducing airway neurogenic inflammation and promoting disease recovery.
文摘背景:运动干预作为经济有效的非物理疗法,可有效上调脑源性神经营养因子表达进而防治帕金森病发生发展,但目前关于靶向脑源性神经营养因子的运动治疗策略在延缓帕金森病发生发展的潜在作用机制尚不明晰。目的:以脑源性神经营养因子和帕金森病的关系为切入点,分析帕金森病病理状态下运动对脑源性神经营养因子表达的特异性调控作用及机制,梳理脑源性神经营养因子介导下不同运动方式对帕金森病的改善效果,并阐明靶向脑源性神经营养因子的运动治疗策略在防治帕金森病的潜在作用机制,旨在为运动防治帕金森病提供新的理论依据。方法:以“帕金森病,脑源性神经营养因子,神经保护,多巴胺,神经元异常凋亡,神经炎症反应,突触可塑性,运动”等为中文检索词;以“Parkinson’s disease,BDNF,Neuroprotection,neuroinflammation,synaptic plasticity”等为英文检索词,分别检索中国知网、万方数据库、PubMed和Web of Science数据库,搜寻各数据库建库至2024年2月发表的所有研究文献,根据纳排标准共获得核心相关文献98篇。结果与结论:①在帕金森病理背景下,运动可通过促进肌因子鸢尾素大量分泌,并降低色氨酸-犬尿氨酸代谢途径紊乱特异性调控脑源性神经营养因子表达。②有氧运动,尤其是特殊有氧运动(动物:旋转杆步行/人类:北欧健走)以及多模式运动可显著上调脑源性神经营养因子表达,进而改善帕金森病的运动症状,此外脑源性神经营养因子还介导身心运动(太极拳)对帕金森病患者认知障碍和睡眠障碍等非运动症状的有效调节。③运动诱导的高表达脑源性神经营养因子可能通过上调抗炎因子白细胞介素10、神经生长因子β和转化生长因子β表达,下调促炎因子肿瘤坏死因子α及白细胞介素1β表达,并抑制核转录因子κB信号通路表达降低小胶质细胞活性减轻神经炎症反应;增加酪氨酸羟化酶活性以促进多巴胺合成释放,并通过下调基质金属蛋白酶3及糖原合成酶激酶3β表达抑制α-突触核蛋白在丝氨酸129位点的磷酸化修饰,以防止神经异常凋亡;诱导突触效能的长时程增强发生,促进突触后致密区蛋白95及突触素大量表达以改善突触可塑性,发挥神经保护作。④鉴于脑源性神经营养因子在帕金森病发病进程及治疗中发挥重要作用,靶向脑源性神经营养因子的运动治疗策略将有助于推动帕金森病疾病“运动+药物”精准医疗的发展。但由于目前研究采用的运动处方较为单一,且研究焦点主要围绕运动症状而缺乏对非运动症状的考察,因此亟待学者采用更加统一和系统的运动处方,围绕非有氧运动类型对同一批帕金森病患者进行长期纵向跟踪研究,以此完善帕金森病运动防治领域研究的不足。
