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: 的抗炎作用:来自体外和体内研究的证据。 (你提供的原文似乎不完整,冒号前缺少具体内容)

Anti-Inflammatory Effects of : Evidence from In Vitro and In Vivo Studies.

作者信息

Lee Keun Hee, Kim Min Hee, Nam Hae Jeong

机构信息

Department of Clinical Korean Medicine, Graduate School, Kyung Hee University, Seoul 02447, Republic of Korea.

Kapsan Oriental Medicine Clinic, Gyeongju 38203, Republic of Korea.

出版信息

Life (Basel). 2025 Apr 2;15(4):587. doi: 10.3390/life15040587.

Abstract

(HGYGT), a traditional herbal formula, is used to treat inflammatory otorhinolaryngological diseases such as otitis media and sinusitis. In this study, we investigated the anti-inflammatory effects of HGYGT in LPS-stimulated RAW 264.7 cells (in vitro) and a carrageenan (CA)-induced rat paw edema model (in vivo). In LPS-stimulated RAW 264.7 cells, treatment with HGYGT (100 and 300 μg/mL) significantly reduced nitric oxide (NO) production by 24.5% and 51.3%, respectively ( < 0.05, < 0.01). It also significantly suppressed the production of PGE2 (49.8%), IL-1β (42.7%), IL-6 (45.6%), and TNF-α (47.2%) at 300 μg/mL ( < 0.01). A Western blot analysis confirmed that HGYGT (300 μg/mL) significantly downregulated iNOS and COX-2 expression by 58.4% and 53.1%, respectively, while COX-1 remained unaffected. And HGYGT treatment at 300 μg/mL markedly inhibited NF-κB activation by 44.9% ( < 0.01). Furthermore, HGYGT selectively inhibited JNK phosphorylation by 46.7% ( < 0.01), without significantly affecting ERK1/2 or p38 MAPKs. In the CA-induced rat paw edema model, oral administration of HGYGT (1.0 g/kg) reduced paw swelling by 31.5% at 4 h post-injection ( < 0.01) and significantly decreased iNOS expression in inflamed paw tissues by 43.2% ( < 0.01). A histological analysis revealed that HGYGT (1.0 g/kg) reduced inflammatory cell infiltration by 39.6% in the affected tissue ( < 0.05), demonstrating its anti-inflammatory potential. Our findings demonstrate that HGYGT exerts anti-inflammatory effects by suppressing the JNK and NF-κB signaling pathways in LPS-stimulated RAW 264.7 cells, reducing the production of inflammatory mediators. Notably, HGYGT selectively inhibits COX-2 without affecting COX-1 and preferentially suppresses the JNK pathway. Moreover, its in vivo anti-inflammatory effects were confirmed through iNOS inhibition and histopathological analysis. These findings provide robust scientific evidence supporting the traditional use of HGYGT and its anti-inflammatory properties.

摘要

(HGYGT)是一种传统草药配方,用于治疗诸如中耳炎和鼻窦炎等炎性耳鼻喉疾病。在本研究中,我们调查了HGYGT在脂多糖(LPS)刺激的RAW 264.7细胞(体外)和角叉菜胶(CA)诱导的大鼠足爪水肿模型(体内)中的抗炎作用。在LPS刺激的RAW 264.7细胞中,用HGYGT(100和300μg/mL)处理分别使一氧化氮(NO)生成显著降低了24.5%和51.3%(<0.05,<0.01)。在300μg/mL时,它还显著抑制了前列腺素E2(PGE2)(49.8%)、白细胞介素-1β(IL-1β)(42.7%)、白细胞介素-6(IL-6)(45.6%)和肿瘤坏死因子-α(TNF-α)(47.2%)的生成(<0.01)。蛋白质免疫印迹分析证实,HGYGT(300μg/mL)分别使诱导型一氧化氮合酶(iNOS)和环氧化酶-2(COX-2)表达显著下调58.4%和53.1%,而环氧化酶-1(COX-1)不受影响。300μg/mL的HGYGT处理显著抑制核因子-κB(NF-κB)激活达44.9%(<0.01)。此外,HGYGT选择性抑制应激活化蛋白激酶(JNK)磷酸化达46.7%(<0.01),而对细胞外信号调节激酶1/2(ERK1/2)或p38丝裂原活化蛋白激酶(MAPKs)无显著影响。在CA诱导的大鼠足爪水肿模型中,口服HGYGT(1.0g/kg)在注射后4小时使足爪肿胀减轻31.5%(<0.01),并使发炎足爪组织中的iNOS表达显著降低43.2%(<0.01)。组织学分析显示,HGYGT(1.0g/kg)使受影响组织中的炎性细胞浸润减少39.6%(<0.05),证明了其抗炎潜力。我们的研究结果表明,HGYGT通过抑制LPS刺激的RAW 264.7细胞中的JNK和NF-κB信号通路发挥抗炎作用,减少炎性介质的生成。值得注意的是,HGYGT选择性抑制COX-2而不影响COX-1,并优先抑制JNK途径。此外,通过iNOS抑制和组织病理学分析证实了其体内抗炎作用。这些发现为支持HGYGT的传统用途及其抗炎特性提供了有力的科学证据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb8d/12028476/a1782ceeaf02/life-15-00587-g001.jpg

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