New insights into effects of Kaixin Powder on depression via lipid metabolism related adiponectin signaling pathway

doi:https://doi.org/10.1016/j.chmed.2022.06.012

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Archive > Volume 15 Issue 2 > 2023,15(2):240-250. DOI:https://doi.org/10.1016/j.chmed.2022.06.012 Prev Next

開心散通過(guò)脂聯(lián)素信號(hào)通路調(diào)節(jié)脂質(zhì)代謝發(fā)揮抗抑郁作用新機(jī)制

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New insights into effects of Kaixin Powder on depression via lipid metabolism related adiponectin signaling pathway

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摘要:

目的：為了闡明開心散的抗抑郁作用機(jī)制，我們進(jìn)行了轉(zhuǎn)錄組學(xué)分析。方法：我們對(duì)抑郁大鼠的海馬進(jìn)行了轉(zhuǎn)錄組學(xué)和KEGG信號(hào)通路分析，進(jìn)一步驗(yàn)證了顯著差異表達(dá)基因，并測(cè)定了血清脂質(zhì)譜的濃度。此外，我們還構(gòu)建了高脂飲食誘導(dǎo)敘利亞金黃地鼠產(chǎn)生類似抑郁行為的動(dòng)物模型，用以驗(yàn)證從轉(zhuǎn)錄組學(xué)分析中獲得的分子機(jī)制。結(jié)果：轉(zhuǎn)錄組學(xué)分析結(jié)果顯示，慢性輕度應(yīng)激大鼠中的24個(gè)差異表達(dá)基因在服用開心散治療兩周后可以得到逆轉(zhuǎn)。開心散治療抑郁癥的主要機(jī)制涉及脂質(zhì)代謝、突觸功能和炎癥等。開心散可以調(diào)節(jié)高脂飲食誘導(dǎo)類似抑郁樣行為中的脂質(zhì)調(diào)節(jié)失衡。此外，開心散還可以改善膽固醇代謝障礙，這可能與AdipoR1-BDNF共調(diào)節(jié)途徑有關(guān)。結(jié)論：總之，我們的研究結(jié)果表明，開心散不僅通過(guò)傳統(tǒng)的心理疾病治療相關(guān)靶點(diǎn)緩解抑郁癥狀，還可能通過(guò)調(diào)節(jié)膽固醇代謝和脂聯(lián)素信號(hào)通路發(fā)揮其抗抑郁作用。

Abstract:

Objective: To clarify the anti-depressive potential mechanisms of Kaixin Powder (KP), a drug that helps to prevent and treat depression and other mentaldiseases, from genome-wide transcriptome profiling. Methods: Transcriptome and KEGG pathway analysis were conducted on the hippocampus of depressed rats, then the differentially expressed genes were validated and serum concentration of lipid parameters were identified by enzymatic assays. Furthermore, high-fat diets induced depression-like behaviors in Syrian golden hamsters were conducted to verify the predicted molecular mechanisms acquired from the transcriptome analysis. Results: Transcriptome results revealed that the 24 differentially expressed genes (DEGs) in chronic mild stress (CMS) rats could be reversed after two weeks of KP treatment. The mechanisms of KP in treating depression firstly involved the regulation of several pathology modules, including lipid metabolism, synapse function and inflammation. KP could regulate imbalances of lipid homeostasis in high-fat diet induced depressive symptoms. Furthermore, it was validated that cholesterol metabolism dysfunction can be ameliorated by KP, which was correlated with upregulation of the AdipoR1-BDNF (brain-derived neurotrophic factor) co-regulatory pathway. Conclusion: Taken together, our results demonstrated that KP not only alleviates depression via traditional mental illness targets, but it may also simulates the cholesterol metabolism and adiponectin signaling with multi-target characteristics.

關(guān)鍵詞:

脂聯(lián)素;膽固醇代謝;抑郁癥;高脂飲食;開心散;轉(zhuǎn)錄組學(xué)分析

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The present study was supported by National Natural Science Foundation of China (No. 81573876 and 81973502).

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