Departamento de Farmacobiología, Centro Universitario de Ciencias Exactas e Ingenierías, Universidad de Guadalajara, Guadalajara, Jalisco, Mexico.
Departamento de Ciencias de la Tierra y de la Vida, Centro Universitario de los Lagos, Universidad de Guadalajara. Lagos de Moreno, Jalisco, Mexico.
Int Immunopharmacol. 2021 Apr;93:107341. doi: 10.1016/j.intimp.2020.107341. Epub 2021 Jan 22.
Although acute stress generally exerts positive effects on the immune system, chronic stress typically causes immunosuppression via the hypothalamic-pituitary-adrenal (HPA) axis. In this study, the effects of capsaicin (1.28 mg/kg intraperitoneally [i.p.] for 7 days) on immune parameters were evaluated under conditions of chronic stress. Capsaicin treatment significantly increased the immune response as evaluated by the delayed-type hypersensitivity (DTH) reaction to dinitrofluorobenzene (DNFB) and splenocyte proliferation assays- It also is able to rescue the splenocytes of the apoptosis induced by stress. The capsaicin treatment increased the production of Th1 cytokines and decreased the production of Th2 cytokines and TGF-β1 in the plasma and culture supernatants of immunosuppressed mice, which is associated with the modulation of Th2 induced by stress cells. Moreover, the production of corticosterone significantly decreased in capsaicin-treated animals as compared to control groups. The capsaicin treatment further attenuated the immunosuppression induced by the corticosterone treatment (40 mg/kg i.p. for 7 days), albeit less potently, as exhibited in the DTH response. Intriguingly, the capsaicin treatment decreased the induction of IL-10, IL-4, and TGF-β1 through high doses of corticosterone, indicating direct cellular immunomodulation. These results show, that capsaicin is able to modulate chronic stress-induced immunosuppression, mediating corticosterone released inhibition, but also, that capsaicin significantly modulates the pharmacological action of corticosterone in vivo.
虽然急性应激通常对免疫系统产生积极影响，但慢性应激通常通过下丘脑-垂体-肾上腺 (HPA) 轴导致免疫抑制。在这项研究中，评估了辣椒素（1.28 mg/kg 腹腔内 [i.p.] 给药 7 天）在慢性应激条件下对免疫参数的影响。辣椒素治疗可显著增加迟发型超敏反应 (DTH) 对二硝基氟苯 (DNFB) 和脾细胞增殖试验的免疫反应-它还能够挽救应激诱导的脾细胞凋亡。辣椒素治疗增加了 Th1 细胞因子的产生，减少了血浆和免疫抑制小鼠培养上清液中 Th2 细胞因子和 TGF-β1 的产生，这与应激细胞中 Th2 诱导的调节有关。此外，与对照组相比，辣椒素治疗动物的皮质酮产生显著减少。尽管作用较弱，但辣椒素治疗进一步减弱了皮质酮治疗（40 mg/kg i.p. 给药 7 天）诱导的免疫抑制，如 DTH 反应所示。有趣的是，辣椒素治疗通过大剂量皮质酮降低了 IL-10、IL-4 和 TGF-β1 的诱导，表明直接的细胞免疫调节。这些结果表明，辣椒素能够调节慢性应激诱导的免疫抑制，介导皮质酮释放抑制，但也表明辣椒素在体内显著调节皮质酮的药理学作用。
