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芍药苷通过调节炎症和抗炎细胞因子的平衡抑制过敏性接触性皮炎小鼠的炎症反应。

Paeoniflorin inhibits inflammatory responses in mice with allergic contact dermatitis by regulating the balance between inflammatory and anti-inflammatory cytokines.

机构信息

Institute of Clinical Pharmacology, Anhui Medical University, Key Laboratory of Anti-inflammatory and Immune Medicine, Ministry of Education, Hefei, 230032, China.

出版信息

Inflamm Res. 2013 Dec;62(12):1035-44. doi: 10.1007/s00011-013-0662-8. Epub 2013 Oct 5.

DOI:10.1007/s00011-013-0662-8
PMID:24096935
Abstract

OBJECTIVE

Paeoniflorin (Pae) was previously reported to inhibit inflammation in the skin of mice with allergic contact dermatitis (ACD); however, the mechanism remains unclear. The primary purpose of this study was to investigate the effect of Pae on the regulation of cytokine production in a murine model of ACD.

METHODS

ACD was induced in the mice by repeated application of dinitrochlorobenzene (DNCB) to their skin. Cutaneous inflammation was evaluated by measuring ear swelling and by histological examination. The cytokine levels were measured by enzyme-linked immunosorbent assays.

RESULTS

The results showed that topical application of DNCB caused obvious swelling and inflammatory cell infiltration. Treatment with Pae (70 or 140 mg/kg/d) significantly inhibited the cutaneous inflammation and decreased thymocyte proliferation in the mice with ACD. Additional data indicated that Pae increased interleukin-4 (IL-4) and IL-10 production but reduced IL-2 and IL-17 levels in the serum as well as in thymocyte and splenocyte culture supernatants. As expected, IL-2 and IL-17 levels in the serum displayed a significant positive correlation with the severity of skin inflammation. In contrast, IL-4 and IL-10 levels were negatively correlated with the inflammation.

CONCLUSIONS

The anti-inflammatory action of Pae in the murine model of ACD may be related to its regulation of an imbalanced cytokine production.

摘要

目的

先前有研究报道芍药苷(Pae)可抑制变应性接触性皮炎(ACD)小鼠皮肤的炎症反应;然而,其作用机制尚不清楚。本研究的主要目的是探讨芍药苷对 ACD 小鼠模型细胞因子产生调节的影响。

方法

通过对小鼠皮肤反复涂抹二硝基氯苯(DNCB)诱导 ACD。通过测量耳肿胀和组织学检查评估皮肤炎症。采用酶联免疫吸附试验检测细胞因子水平。

结果

结果表明,DNCB 局部应用可导致明显的肿胀和炎性细胞浸润。芍药苷(70 或 140mg/kg/d)治疗可显著抑制 ACD 小鼠的皮肤炎症和胸腺细胞增殖。进一步的研究表明,芍药苷可增加白细胞介素-4(IL-4)和白细胞介素-10(IL-10)的产生,但降低白细胞介素-2(IL-2)和白细胞介素-17(IL-17)水平,无论是在血清还是在胸腺细胞和脾细胞培养上清液中。如预期的那样,血清中 IL-2 和 IL-17 水平与皮肤炎症的严重程度呈显著正相关。相反,IL-4 和 IL-10 水平与炎症呈负相关。

结论

芍药苷在 ACD 小鼠模型中的抗炎作用可能与其调节细胞因子产生失衡有关。

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