[Mechanism of Cyanotis arachnoidea Gel in improving melasma based on network pharmacology and transcriptomics].

Q3 Pharmacology, Toxicology and Pharmaceutics
Mamattursun Marziya, Li-Ying Qiu, Wan-Quan Bai, Amar Dlraba, Chen Ma, Le Zhang, Jian Gu
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引用次数: 0

Abstract

Through a comprehensive analysis combining network pharmacology prediction and transcriptomics, this study systematically explained the multi-target mechanism of Cyanotis arachnoidea(CA) Gel in improving melasma. A melasma model was induced in female SD rats by progesterone injection combined with ultraviolet B(UVB) irradiation for 40 consecutive days, while the blank control group was only fed routinely. After successful model establishment, the rats were randomly divided into five groups and administered different doses of CA ethanol extract gel(high, medium, and low doses) or arbutin Gel(positive control), which were applied once daily for 28 consecutive days. Subsequently, the levels of superoxide dismutase(SOD), malondialdehyde(MDA), and tyrosinase(TYR) in the skin, serum, and liver tissues were measured. Hematoxylin-eosin(HE) staining and Masson-Fontana staining were used to observe the pathological changes in the tissues. Network pharmacology combined with transcriptomics was employed to identify core targets and pathways, and the differential gene expression was validated by quantitative real-time PCR(qPCR). Pharmacodynamic experiments showed that CA Gel significantly increased SOD activity and decreased MDA and TYR levels in the skin, serum, and liver of model rats. It also improved epidermal thickening, inflammatory infiltration, collagen loss, and melanin deposition. Network pharmacology analysis showed that CA mainly regulated core targets such as signal transducer and activator of transcription 3(STAT3), epidermal growth factor receptor(EGFR), and interleukin-6(IL-6), and modulated the phosphatidylinositol 3-kinase(PI3K)-protein kinase B(AKT) and interleukin-17(IL-17) signaling pathways. Transcriptomic analysis showed that CA Gel significantly downregulated the gene expression of heat shock protein 90β family member 1(Hsp90b1), heat shock protein 90α family member 1(Hsp90aa1), and the key steroid synthesis enzyme cytochrome P450 family 17 subfamily A member 1(Cyp17a1), while upregulating thioredoxin 1(Txn1). qPCR results confirmed that CA Gel regulated oxidative stress and inflammatory response by inhibiting the IL-17 signaling pathway and steroid hormone synthesis. This study, for the first time, reveals the molecular mechanism of CA Gel in improving melasma through multi-target synergistic regulation of oxidative stress, inflammatory response, and hormone metabolism pathways, providing a scientific basis for the treatment of pigmentation diseases with traditional Chinese medicine.

[基于网络药理学和转录组学的蛛网膜蓝藻凝胶改善黄褐斑的机制]。
本研究通过网络药理学预测与转录组学相结合的综合分析,系统地解释了Cyanotis arachnoidea(CA)凝胶改善黄褐斑的多靶点机制。采用黄体酮注射联合紫外线B(UVB)连续照射40 d的方法建立SD雌性大鼠黄褐斑模型,空白对照组仅常规喂养。造模成功后,将大鼠随机分为5组,分别给予不同剂量的CA乙醇提取物凝胶(高、中、低剂量)或熊果苷凝胶(阳性对照),每天1次,连续28 d。随后,测量皮肤、血清和肝脏组织中超氧化物歧化酶(SOD)、丙二醛(MDA)和酪氨酸酶(TYR)的水平。采用苏木精-伊红(HE)染色、Masson-Fontana染色观察组织病理变化。采用网络药理学与转录组学相结合的方法鉴定核心靶点和通路,并通过实时荧光定量PCR(qPCR)验证差异基因的表达。药效学实验表明,CA凝胶可显著提高模型大鼠皮肤、血清和肝脏中SOD活性,降低MDA和TYR水平。它还能改善表皮增厚、炎症浸润、胶原蛋白流失和黑色素沉积。网络药理学分析表明,CA主要调控信号传导和转录激活因子3(STAT3)、表皮生长因子受体(EGFR)、白介素-6(IL-6)等核心靶点,调节磷脂酰肌醇3-激酶(PI3K)-蛋白激酶B(AKT)和白介素-17(IL-17)信号通路。转录组学分析显示,CA凝胶显著下调热休克蛋白90β家族成员1(Hsp90b1)、热休克蛋白90α家族成员1(Hsp90aa1)和关键类固醇合成酶P450家族17亚家族A成员1(Cyp17a1)的基因表达,上调硫氧还蛋白1(Txn1)的基因表达。qPCR结果证实CA凝胶通过抑制IL-17信号通路和类固醇激素合成调节氧化应激和炎症反应。本研究首次揭示了CA凝胶通过多靶点协同调节氧化应激、炎症反应、激素代谢途径改善黄褐斑的分子机制,为中药治疗色素沉着病提供科学依据。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Zhongguo Zhongyao Zazhi
Zhongguo Zhongyao Zazhi Pharmacology, Toxicology and Pharmaceutics-Pharmacology, Toxicology and Pharmaceutics (all)
CiteScore
1.50
自引率
0.00%
发文量
581
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