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从臭椿中的芦丁-7-O-葡萄糖苷通过下调辅助性 T 细胞细胞因子表达和抑制前列腺素 E2 产生抑制卵清蛋白诱导的哮喘模型中的抗哮喘活性。

Antiasthmatic activity of luteolin-7-O-glucoside from Ailanthus altissima through the downregulation of T helper 2 cytokine expression and inhibition of prostaglandin E2 production in an ovalbumin-induced asthma model.

机构信息

Yeungnam University, Gyeongsan, Republic of Korea.

出版信息

Biol Pharm Bull. 2009 Sep;32(9):1500-3. doi: 10.1248/bpb.32.1500.

DOI:10.1248/bpb.32.1500
PMID:19721222
Abstract

Previously, we reported that an ethanol extract of Ailanthus altissima has antiinflammatory activity in an ovalbumin (OVA)-sensitized murine asthmatic model. To determine the biological compounds from this plant, luteolin-7-O-glucoside (L7G) was isolated and its antiasthmatic activity was evaluated in an in vivo murine asthmatic model. L7G (10 to 100 mg/kg, per os (p.o.)) reduced the amount of eosinophil infiltration in bronchoalveolar lavage (BAL) fluid in a dose-dependent manner. In comparison, dexamethasone (5 mg/kg, p.o.), which was used as a positive control, also strongly inhibited the number of infiltrating eosinophils. L7G inhibited both the prostaglandin E(2) (PGE(2)) and serum immunoglobulin E level in BAL fluid in a dose-dependent manner. In addition, L7G inhibited the transcript profiles of interleukin (IL)-4, IL-5, and IL-13 mRNA expression levels in the murine asthma model, as determined using reverse transcription-polymerase chain reaction (RT-PCR). These results suggest that the antiasthmatic activity of L7G in OVA-induced lung inflammation may occur in part via the downregulation of T helper 2 cytokine transcripts as well as the inhibition of PGE(2) production.

摘要

先前,我们报道过臭椿乙醇提取物在卵清蛋白(OVA)致敏的哮喘小鼠模型中具有抗炎活性。为了确定该植物中的生物化合物,分离出了芦丁-7-O-葡萄糖苷(L7G),并在体内哮喘小鼠模型中评价了其抗哮喘活性。L7G(10 至 100mg/kg,口服(p.o.))呈剂量依赖性地减少支气管肺泡灌洗液(BAL)中嗜酸性粒细胞浸润的量。相比之下,作为阳性对照的地塞米松(5mg/kg,p.o.)也强烈抑制了浸润嗜酸性粒细胞的数量。L7G 呈剂量依赖性地抑制 BAL 液中前列腺素 E2(PGE2)和血清免疫球蛋白 E 水平。此外,L7G 通过逆转录聚合酶链反应(RT-PCR)抑制了哮喘小鼠模型中白细胞介素(IL)-4、IL-5 和 IL-13mRNA 表达水平的转录谱。这些结果表明,L7G 在 OVA 诱导的肺部炎症中的抗哮喘活性可能部分通过下调辅助性 T 细胞细胞因子转录本以及抑制 PGE2 的产生来实现。

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