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首页> 外文期刊>Food & Function >The protective effect of Sargassum horneri against particulate matter-induced inflammation in lung tissues of an in vivo mouse asthma model
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The protective effect of Sargassum horneri against particulate matter-induced inflammation in lung tissues of an in vivo mouse asthma model

机译：Sargassum Horneri对体内小鼠哮喘模型肺组织颗粒状物质炎症的保护作用

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摘要

Sargassum horneri is an edible brown seaweed with potential anti-inflammatory properties. The present study was designed to evaluate the anti-inflammatory properties of S. horneri using an in vivo mouse asthma model following exposure to particulate matter (PM). 7-8 week old BALB/c mice (20-25 g) were randomly divided into seven groups (n = 4) as follows: 1: no treatment, 2: OVA (ovalbumin) + PM, 3: OVA + PM + SHE (S. horneri ethanol extract) 200 mg kg(-1), 4: OVA + PM + SHE 400 mg kg(-1), 5: OVA + PM + prednisone 5 mg kg(-1), 6: OVA only, and 7: PM only. All mice (except healthy controls) were sensitized on the first day by intraperitoneal injection of 10 mu g OVA and 2 mg Al(OH)(3) in 200 mu L of saline. Starting from day 15, mice (except groups 1 and 6) were exposed to sonicated PM (5 mg m(-3), 30 min day(-1)) through a nebulizer daily for 7 consecutive days. Mice exposed to PM and OVA showed up-regulated expression of MAPKs and pro-inflammatory cytokine production in the lungs. Furthermore, PM-exposed lungs had significantly reduced expression of Nrf2 and HO-1 genes. However, oral administration of the SHE reduced the phosphorylation levels of MAPKs, iNOS and COX2 expression levels, and mRNA expression levels of pro-inflammatory cytokines. In addition, SHE treated group mice had up-regulated anti-oxidant gene expression levels in the lungs compared to group 2. These findings demonstrate that oral administration of the SHE re-establishes PM-induced inflammation and oxidative stress in the lungs. Taken together, the SHE has therapeutic potential in preventing PM-induced inflammation and oxidative stress.
机译：Sargassum Horneri是一种可食用的棕色海藻，具有潜在的抗炎性质。本研究旨在评估在暴露于颗粒物质（PM）后使用体内小鼠哮喘模型进行S. Horneri的抗炎特性。 7-8周龄旧的BALB / C小鼠（20-25g）随机分为7组（n = 4），如下：1：无治疗，2：OVA（卵烧）+ PM，3：OVA + PM +她（S. Horneri乙醇提取物）200 mg kg（-1），4：ova + Pm + She 400 mg kg（-1），5：ova + pm +泼尼松5 mg kg（-1），6：ova，和7：下午。所有小鼠（健康对照除外）通过腹腔注射10μgova和200μg盐水中的2mg（oh）（3），致敏。从第15天开始，通过雾化剂连续7天将小鼠（第1组和第6组除外）暴露于超声处理的PM（5mg m（-3），30分钟（-1））。暴露于PM和OVA的小鼠显示出肺中MAPK和促炎细胞因子产生的上调表达。此外，PM暴露的肺部显着降低了NRF2和HO-1基因的表达。然而，口服给予她的映射水平的映射水平的映射水平，伊克斯和COX2表达水平，以及促炎细胞因子的mRNA表达水平。此外，与第2组相比，她治疗的群体小鼠对肺部有上调的抗氧化基因表达水平。这些研究结果表明，她们的口服给药在肺部重新建立PM诱导的炎症和氧化胁迫。连同，她在预防PM诱导的炎症和氧化应激方面具有治疗潜力。

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