炮制对栀子抗抑郁作用的影响及其机制研究
Anti-Depressant Effect and Its Mechanism of Gardenia Jasminoides Ellis Before and After Processing
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摘要: 目的 以栀子不同炮制品为研究对象,比较不同炮制品栀子抗抑郁作用及其机制。方法 建立慢性不可预知性应激(CUMS)小鼠模型,并采用栀子不同炮制品水提物干预;给药结束后,采用行为学评价其抗抑郁作用的差异,并探讨其分子学机制。结果 与模型组相比,炒、焦、生栀子组小鼠糖水消耗显著升高(P<0.01);炒、焦栀子明显降低悬尾试验(P<0.05)和强迫游泳试验(P<0.05~0.01)的不动时间,生栀子对以上2者无显著改善;小鼠海马组织中炎性因子白细胞介素-1β(IL-1β)、肿瘤坏死因子-α(TNF-α),磷酸化核因子-κB(p-NF-κB)(P<0.01)以及胶质纤维酸性蛋白(GFAP)(P<0.01)的表达在造模后显著上升,炮制后栀子(炒、焦)抗炎作用优于生栀子。其中炒栀子抗炎作用最优,IL-β、TNF-α和GFAP均能被炒栀子显著下调(P<0.01)。结论 栀子不同炮制品抗抑郁作用存在差异,其抗抑郁作用差异与其调节小鼠海马组织中炎性因子IL-1β、TNF-α等以及GFAP的表达有关。Abstract: OBJECTIVE To investigate the difference of anti-depressant effect between different processed products of Gardenia jasminoides Ellis, and to explore the mechanism. METHODS Chronic unpredictable mild stress model was established and water extract of different processed products of Gardenia jasminoides Ellis was used for administration. Behavioral tests were used to evaluate the difference of anti-depressant effect between different processed products of Gardenia jasminoides Ellis, and the molecular mechanism was further explored. RESULTS The immobility time of TST (P<0.05) and FST (P<0.05,P<0.01) was significantly reduced by CZZ and JZZ while there was no significant improvement in TST and FST in SZZ group. As expected, the expressions of IL-1β,TNF-α, p-NF-κB and GFAP were obviously higher in model group (P<0.01) than those in CZZ and JZZ. CZZ had the best anti-inflammatory effect by significantly decreasing the expressions of IL-1β, TNF-α and GFAP. CONCLUSION The anti-depressant effects of different processed products of Gardenia jasminoides Ellis are different. It is assumed that the mechanism of the anti-depressant effects and its difference is related to the regulation of the expression of IL-1β, TNF-α and GFAP in the hippocampal tissue of mice.
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Key words:
- Gardenia jasminoides Ellis /
- anti-depressant effect /
- processing /
- CUMS /
- inflammatory factors
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[1] RIZZO LB, SWARDFAGER W, MAURYA PK, et al. An immunological age index in bipolar disorder: A confirmatory factor analysis of putative immunosenescence markers and associations with clinical characteristics[J]. Int J Methods Psychiatr Res, 2018, 27(4): e1614. [2] DUFFY A,HORROCKS J, DOUCETTE S, et al. Immunological and neurotrophic markers of risk status and illness development in high-risk youth: Understanding the neurobiological underpinnings of bipolar disorder[J]. Int J Bipolar Disord, 2014, 2(1): 29. [3] MODABBERNIA A, TASLIMI S, BRIETZKE E, et al. Cytokine alterations in bipolar disorder: A meta-analysis of 30 studies[J]. Biol Psychiatry, 2013, 74(1): 15-25. [4] NOTO C, RIZZO LB, MANSUR RB, et al. Targeting the inflammatory pathway as a therapeutic tool for major depression[J]. Neuroimmunomodulation, 2014, 21(2/3): 131-139. [5] LEONARD B, MAES M. Mechanistic explanations how cell-mediated immune activation, inflammation and oxidative and nitrosative stress pathways and their sequels and concomitants play a role in the pathophysiology of unipolar depression[J]. Neurosci Biobehav Rev, 2012, 36(2): 764-785. [6] PEARSON-LEARY J, EACRET D, CHEN R, et al. Inflammation and vascular remodeling in the ventral hippocampus contributes to vulnerability to stress[J]. Transl Psychiatry, 2017, 7(6): e1160. [7] SLAVICH GM, IRWIN MR. From stress to inflammation and major depressive disorder: A social signal transduction theory of depression.[J]. Psychol Bull, 2014, 140(3): 774-815. [8] RIAL D, LEMOS C, PINHEIRO H, et al. Depression as a glial-based synaptic dysfunction[J]. Front Cell Neurosci, 2015, 9: 521. [9] ROSENBAUM C, SCHICK MA, WOLLBORN J, et al. Activation of myenteric glia during acute inflammation in vitro and in vivo[J]. PLoS ONE, 2016, 11(3): e151335. [10] SHELTON RC, MILLER AH. Eating ourselves to death (and despair): The contribution of adiposity and inflammation to depression[J].Prog Neurobiol, 2010, 91(4): 275-299. [11] 国家药典委员会.中国药典:一部[S].北京:中国医药科技出版社,2015:175-177. [12] 郝文宇,杨楠,高云周,等. 栀子粗提物对抑郁模型小鼠行为学及海马神经发生的影响[J]. 中国比较医学杂志, 2009, 19(10): 11-14. [13] ZHAO C, ZHANG H, LI H, et al. Geniposide ameliorates cognitive deficits by attenuating the cholinergic defect and amyloidosis in middle-aged Alzheimer model mice[J]. Neuropharmacology, 2017, 116: 18-29. [14] XU B, LI YL, XU M. Erratum: Geniposide ameliorates TNBS-induced experimental colitis in rats via reducing inflammatory cytokine release and restoring impaired intestinal barrier function[J]. Acta Pharmacol Sin, 2017, 38(5): 734. [15] 陶伟伟,肖东,吴浩然,等. 基于药对探讨中药复方越鞠丸抗抑郁作用配伍规律[J]. 中国药理学通报, 2018, 34(9): 1314-1320. [16] 朱震亨.丹溪心法[M] .北京:北京市中国书店,1986:215,124, 133. [17] XUE W, WANG W, GONG T, et al. PKA-CREB-BDNF signaling regulated long lasting antidepressant activities of Yueju but not ketamine[J]. Sci Rep, 2016, 6: 26331. [18] MONTEGGIA LM, MALENKA RC, DEISSEROTH K. Depression: The best way forward[J]. Nature, 2014, 515(7526): 200-201. [19] SUN Y, GENG W, PAN Y, et al. Supplementation with Lactobacillus kefiranofaciens ZW3 from Tibetan Kefir improves depression-like behavior in stressed mice by modulating the gut microbiota[J]. Food Funct, 2019, 10(2): 925-937. [20] LIU Y, JIA G, GOU L, et al. Antidepressant-like effects of tea polyphenols on mouse model of chronic unpredictable mild stress[J]. Pharmacol Biochem Behav, 2013, 104: 27-32. [21] PAN Y, HONG Y, ZHANG QY, et al. Impaired hypothalamic insulin signaling in CUMS rats: Restored by icariin and fluoxetine through inhibiting CRF system[J].Psychoneuroendocrinology, 2013, 38(1): 122-134. [22] HANNESTAD J, DELLAGIOIA N, BLOCH M. The effect of antidepressant medication treatment on serum levels of inflammatory cytokines: A meta-analysis[J]. Neuropsychopharmacology, 2011, 36(12): 2452-2459. [23] GOSHEN I, KREISEL T, BEN-MENACHEM-ZIDON O, et al. Brain interleukin-1 mediates chronic stress-induced depression in mice via adrenocortical activation and hippocampal neurogenesis suppression[J].Mol Psychiatry, 2008,13(7):717-728. [24] GUIDA F, TURCO F, IANNOTTA M, et al. Antibiotic-induced microbiota perturbation causes gut endocannabinoidome changes, hippocampal neuroglial reorganization and depression in mice[J]. Brain Behav Immun, 2018, 67: 230-245.
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