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薰衣草精油可预防马拉硫磷诱导的雄性小鼠生殖损伤。

Lavandula stoechas essential oils protect against Malathion-induces reproductive disruptions in male mice.

机构信息

Laboratory Functional Physiology and Bio-resources Valorisation, Higher Institute of Biotechnology of Beja, University of Jendouba, Avenue Habib Bourguiba, BP, 382, 9000, Beja, Tunisia.

出版信息

Lipids Health Dis. 2018 Nov 8;17(1):253. doi: 10.1186/s12944-018-0891-5.

DOI:10.1186/s12944-018-0891-5
PMID:30409133
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6225712/
Abstract

BACKGROUND

The current study was conducted to evaluate the protective effect of Lavandula stoechas essential oils (LSEO) against malathion (M) exposure-caused reprotoxicity in male mice as well as the possible mechanisms implicated in such protection.

METHODS

Six-eight-week-old male mice weighting 25-30 g were used and divided into four groups: normal-control, LSEO (50 mg/kg, b.w.), malathion (200 mg/kg, b.w.) and malathion + LSEO treated mice. Malathion was emulsioned in corn oil and per orally administered for 30 days. LSEO was daily administrated during the same period. LSEO chemical identification was done by Gas chromatography-mass spectrometry (GC-MS). Reproduction-damages and LSEO-benefits were assessed using histopathological, biochemical and steroidogenesis gene expression disruptions and improvements.

RESULTS

The GC-MS analysis, allowed to the identification of 25 bioactive compounds in MCEO. In vivo, we firstly found that malathion exposure induced a clear reprotoxicity as assessed by a significant-decrease (P < 0.05) of testis/epididymis relative weights, serum testosterone level and reproductive performance. Malathion also produced lipoperoxidation, thiol (-SH) groups decrease as well as a significant-depletion (P < 0.05) of antioxidant enzyme activities such as catalase (CAT) and glutathione peroxidase (GPx), total superoxide dismutase (SOD), Cu/Zn-SOD and Mn-SOD in testis and epididymis. The histopathological examination showed marked change in both studied tissues. All these biochemical and structural changes were significantly (P < 0.05) corrected by LSEO co-administration. More importantly, malathion exposure remarkably (P < 0.05) down-regulated the expression of StAR gene as well as, the mRNA levels of P450scc, 3ßHSD and 17ß-HSD, while LSEO-administration strangely protected against steroidogenesis disruption.

CONCLUSIONS

The potential protective effects of LSEO against malathion-induced reprotoxicity and oxidative stress might be partially to its antioxidant properties as well as its opposite effect against some gene expression involved in the steroidogenesis.

摘要

背景

本研究旨在评估薰衣草精油(LSEO)对马拉硫磷(M)暴露引起的雄性小鼠生殖毒性的保护作用,并探讨其可能的保护机制。

方法

使用体重为 25-30g 的 6-8 周龄雄性小鼠,分为 4 组:正常对照组、LSEO(50mg/kg,bw)组、马拉硫磷(200mg/kg,bw)组和马拉硫磷+LSEO 处理组。马拉硫磷用玉米油乳化后口服 30 天。LSEO 在同一时期每天给药。通过气相色谱-质谱联用(GC-MS)分析 LSEO 的化学成分。通过组织病理学、生化和类固醇生成基因表达紊乱和改善来评估生殖损伤和 LSEO 的益处。

结果

GC-MS 分析鉴定出 MCEO 中 25 种具有生物活性的化合物。体内研究发现,马拉硫磷暴露导致生殖毒性,表现为睾丸/附睪相对重量、血清睪酮水平和生殖性能显著降低(P<0.05)。马拉硫磷还导致脂质过氧化、巯基(-SH)减少以及抗氧化酶活性如过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GPx)、总超氧化物歧化酶(SOD)、Cu/Zn-SOD 和 Mn-SOD 在睾丸和附睪中的显著耗竭(P<0.05)。组织病理学检查显示这两种组织都有明显的变化。LSEO 联合给药可显著改善所有这些生化和结构变化(P<0.05)。更重要的是,马拉硫磷暴露显著下调 StAR 基因表达以及 P450scc、3ßHSD 和 17ß-HSD 的 mRNA 水平,而 LSEO 给药则能防止类固醇生成紊乱。

结论

LSEO 对马拉硫磷诱导的生殖毒性和氧化应激的潜在保护作用可能部分与其抗氧化特性以及对某些参与类固醇生成的基因表达的相反作用有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ccc/6225712/04aba9f06c52/12944_2018_891_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ccc/6225712/3132896e5cff/12944_2018_891_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ccc/6225712/6e4bd812cb16/12944_2018_891_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ccc/6225712/1759e9975fd1/12944_2018_891_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ccc/6225712/b2f4ecde600a/12944_2018_891_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ccc/6225712/e1815318b6f1/12944_2018_891_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ccc/6225712/906b0173cbd7/12944_2018_891_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ccc/6225712/04aba9f06c52/12944_2018_891_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ccc/6225712/3132896e5cff/12944_2018_891_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ccc/6225712/6e4bd812cb16/12944_2018_891_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ccc/6225712/1759e9975fd1/12944_2018_891_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ccc/6225712/b2f4ecde600a/12944_2018_891_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ccc/6225712/e1815318b6f1/12944_2018_891_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ccc/6225712/906b0173cbd7/12944_2018_891_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ccc/6225712/04aba9f06c52/12944_2018_891_Fig7_HTML.jpg

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