Tectorigenin通过激活Th2介导的过敏性哮喘小鼠中的Keap1/Nrf2/HO-1信号通路来抑制氧化应激
2024/02/23
摘要
背景：哮喘是一种慢性阻塞性气道疾病，是世界上最常见的非传染性疾病之一。Tectorigenin (Tec)是一种在植物中发现的具有显著抗氧化和抗炎能力的类黄酮。然而，Tec的抗氧化特性尚未在过敏性哮喘中得到证实。
方法：在本研究中，我们建立了一个由卵清蛋白(OVA)诱导的哮喘BALB/c小鼠模型，并用它来评估Tec作为一种可能的治疗药物的疗效。
结果：Tec降低血清ova特异性免疫球蛋白(Ig) E和IgG1分泌水平、支气管肺泡灌洗液(BALF)细胞总数和炎症细胞分布明显减少、肺组织炎症反应减弱。此外，Tec通过增加Th1相关因子(白细胞介素(IL)-12和T-bet)的表达和降低Th2相关因子(IL-4、IL-5、IL-13和GATA结合蛋白3)的表达来调节T辅助1(Th1)/Th2平衡。此外，Tec还能抑制IL-6、肿瘤坏死因子- α、IL-1β等促炎细胞因子。Tec还显著增加了抗氧化剂(过氧化氢酶和超氧化物歧化酶)浓度，同时降低了BALF中氧化应激指标(如活性氧和丙二醛)的强度。最后，Tec有效激活Keap1/Nrf2/HO-1信号通路，阻止上皮-间质转化。
结论：目前的研究结果表明，Tec可能有助于缓解哮喘相关的炎症和氧化应激反应。
Tectorigenin inhibits oxidative stress by activating the Keap1/Nrf2/HO-1 signaling pathway in Th2-mediated allergic asthmatic mice.
Jiang Y, Nguyen TV, Jin J
Abstrast
Background: Asthma is a chronic obstructive airway condition and one of the most common non-communicable illnesses worldwide. Tectorigenin (Tec) is an isoflavonoid found in plants that possesses significant antioxidative and anti-inflammatory abilities. Nevertheless, the antioxidative properties of Tec have not yet been documented in allergic asthma.
Methods: In this study, we created an asthmatic BALB/c mouse model induced by ovalbumin (OVA) and used it to assess the efficacy of Tec as a possible therapy agent.
Results: Tec decreased the serum OVA-specific immunoglobulin (Ig) E and IgG1 secretion levels. The total number of cells and the distribution of inflammatory cells decreased significantly in bronchoalveolar lavage fluid (BALF), with weakened inflammatory reaction in pulmonary tissues. Additionally, Tec regulated the T helper 1(Th1)/Th2 balance by increasing the expression of Th1- related factors (interleukin (IL)-12 and T-bet) and decreasing the expression of Th2-related factors (IL-4, IL-5, IL-13, and GATA binding protein 3. In addition, the pro-inflammatory cytokines such as IL-6, tumor necrosis factor-alpha, and IL-1β were also inhibited by Tec. Tec also dramatically increased antioxidant (catalase and superoxide dismutase) concentrations while lowering the intensity of the indicators of oxidative stress such as reactive oxygen species and malondialdehyde in BALF. Finally, Tec effectively activated the Keap1/Nrf2/HO-1 signaling pathway and prevented the epithelial-mesenchymal transition.
Conclusions: The results of the current study show that Tec may be useful in relieving the inflammatory and oxidative stress responses associated with asthma.
背景：哮喘是一种慢性阻塞性气道疾病，是世界上最常见的非传染性疾病之一。Tectorigenin (Tec)是一种在植物中发现的具有显著抗氧化和抗炎能力的类黄酮。然而，Tec的抗氧化特性尚未在过敏性哮喘中得到证实。
方法：在本研究中，我们建立了一个由卵清蛋白(OVA)诱导的哮喘BALB/c小鼠模型，并用它来评估Tec作为一种可能的治疗药物的疗效。
结果：Tec降低血清ova特异性免疫球蛋白(Ig) E和IgG1分泌水平、支气管肺泡灌洗液(BALF)细胞总数和炎症细胞分布明显减少、肺组织炎症反应减弱。此外，Tec通过增加Th1相关因子(白细胞介素(IL)-12和T-bet)的表达和降低Th2相关因子(IL-4、IL-5、IL-13和GATA结合蛋白3)的表达来调节T辅助1(Th1)/Th2平衡。此外，Tec还能抑制IL-6、肿瘤坏死因子- α、IL-1β等促炎细胞因子。Tec还显著增加了抗氧化剂(过氧化氢酶和超氧化物歧化酶)浓度，同时降低了BALF中氧化应激指标(如活性氧和丙二醛)的强度。最后，Tec有效激活Keap1/Nrf2/HO-1信号通路，阻止上皮-间质转化。
结论：目前的研究结果表明，Tec可能有助于缓解哮喘相关的炎症和氧化应激反应。
(中日友好医院呼吸与危重症医学科 万静萱 摘译 林江涛 审校)
(Free Radic Biol Med. 2024 Feb 20;212;doi: 10.1016/j.freeradbiomed.2023.12.031.IF: 6.17)
(Free Radic Biol Med. 2024 Feb 20;212;doi: 10.1016/j.freeradbiomed.2023.12.031.IF: 6.17)
Tectorigenin inhibits oxidative stress by activating the Keap1/Nrf2/HO-1 signaling pathway in Th2-mediated allergic asthmatic mice.
Jiang Y, Nguyen TV, Jin J
Abstrast
Background: Asthma is a chronic obstructive airway condition and one of the most common non-communicable illnesses worldwide. Tectorigenin (Tec) is an isoflavonoid found in plants that possesses significant antioxidative and anti-inflammatory abilities. Nevertheless, the antioxidative properties of Tec have not yet been documented in allergic asthma.
Methods: In this study, we created an asthmatic BALB/c mouse model induced by ovalbumin (OVA) and used it to assess the efficacy of Tec as a possible therapy agent.
Results: Tec decreased the serum OVA-specific immunoglobulin (Ig) E and IgG1 secretion levels. The total number of cells and the distribution of inflammatory cells decreased significantly in bronchoalveolar lavage fluid (BALF), with weakened inflammatory reaction in pulmonary tissues. Additionally, Tec regulated the T helper 1(Th1)/Th2 balance by increasing the expression of Th1- related factors (interleukin (IL)-12 and T-bet) and decreasing the expression of Th2-related factors (IL-4, IL-5, IL-13, and GATA binding protein 3. In addition, the pro-inflammatory cytokines such as IL-6, tumor necrosis factor-alpha, and IL-1β were also inhibited by Tec. Tec also dramatically increased antioxidant (catalase and superoxide dismutase) concentrations while lowering the intensity of the indicators of oxidative stress such as reactive oxygen species and malondialdehyde in BALF. Finally, Tec effectively activated the Keap1/Nrf2/HO-1 signaling pathway and prevented the epithelial-mesenchymal transition.
Conclusions: The results of the current study show that Tec may be useful in relieving the inflammatory and oxidative stress responses associated with asthma.
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哮喘COPD重叠患者上调的微小RNA-125b-5p通过靶向IL6R/TRIAP1信号介导氧化应激和晚期细胞凋亡
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