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1.重庆三峡医药高等专科学校中医学院,重庆 404000
2.重庆三峡医药高等专科学校附属中医院急诊重症医学科,重庆 404000
3.重庆三峡医药高等专科学校附属中医院妇产科,重庆 404000
4.重庆三峡医药高等专科学校附属中医院内分泌科,重庆 404000
5.重庆三峡医药高等专科学校附属中医院肾病科,重庆 404000
副教授。研究方向:中医内科疾病诊疗。E-mail:76193263@qq.com
主任医师。研究方向:中医药治疗常见病的相关研究。E-mail:791915121@qq.com
收稿:2025-12-05,
修回:2026-03-04,
录用:2026-03-09,
纸质出版:2026-04-15
移动端阅览
于鹏龙,邓建青,孙善红,等.铁皮石斛对干皮症小鼠皮肤损伤的改善作用及机制 [J].中国药房,2026,37(07):914-919.
YU Penglong,DENG Jianqing,SUN Shanhong,et al.Improvement effect and mechanism of Dendrobium officinale on skin damage in mice with xeroderma[J].ZHONGGUO YAOFANG,2026,37(07):914-919.
于鹏龙,邓建青,孙善红,等.铁皮石斛对干皮症小鼠皮肤损伤的改善作用及机制 [J].中国药房,2026,37(07):914-919. DOI: 10.6039/j.issn.1001-0408.2026.07.15.
YU Penglong,DENG Jianqing,SUN Shanhong,et al.Improvement effect and mechanism of Dendrobium officinale on skin damage in mice with xeroderma[J].ZHONGGUO YAOFANG,2026,37(07):914-919. DOI: 10.6039/j.issn.1001-0408.2026.07.15.
目的
2
研究铁皮石斛对干皮症小鼠皮肤损伤的改善作用及机制。
方法
2
将小鼠随机分为对照组、模型组、铁皮石斛组,每组5只。除对照组(仅做剃毛处理)外,其余各组小鼠采用丙酮-乙醚混合液复制干皮症模型,连续造模5 d。铁皮石斛组小鼠于每天第1次造模后2 h时,涂抹200 μL铁皮石斛混悬液(0.2 mg/mL),对照组和模型组小鼠涂抹等体积纯水,每天1次,直至造模结束。末次给药后,观察小鼠皮肤损伤情况和病理学形态;采用免疫荧光法检测小鼠皮肤组织中聚丝蛋白(Filaggrin)、兜甲蛋白(Loricrin)、增殖细胞核抗原Ki67蛋白表达水平;采用16S rRNA测序法联合基因本体和京都基因与基因组百科全书(KEGG)富集分析筛选铁皮石斛对干皮症皮肤损伤改善作用的核心通路,并进行验证。
结果
2
与对照组比较,模型组小鼠有明显的搔抓行为,皮肤有大量鳞屑,表皮角化过度、棘层肥厚;皮肤鳞屑评分、表皮厚度和皮肤组织中Ki67、Filaggrin、Loricrin蛋白表达水平均显著增加/升高(
P
<0.05);与模型组比较,铁皮石斛组小鼠搔抓行为和鳞屑减少,皮肤角化程度减轻,上述定量指标显著减小/降低(
P
<0.05)。核心通路筛选结果显示,差异基因涉及的KEGG通路包括白细胞介素17(IL-17)、肿瘤坏死因子(TNF)等信号通路;进一步验证实验发现,经铁皮石斛干预后,小鼠皮肤组织中IL-17、TNF信号通路下游效应分子CCN1、Hbegf、Tnfrsf12a、Thbs1的mRNA表达水平均显著降低(
P
<0.05)。
结论
2
铁皮石斛可修复干皮症小鼠皮肤损伤;其作用机制与恢复角质形成细胞的增殖与分化平衡,下调CCN1、Hbegf、Tnfrsf12a、Thbs1 mRNA表达有关。
OBJECTIVE
2
To study the improvement effect and mechanism of
Dendrobium officinale
on skin damage in mice with xeroderma.
METHODS
2
The mice were randomly divided into control group, model group,
and
D. officinale
group, with 5 mice in each group. Except for the control group (which only underwent shaving treatment), the mice in all other groups were induced to develop a xeroderma model using an acetone-ether mixture for five consecutive days. The mice in
D. officinale
group were treated with 200 μL of
D. officinale
suspension (0.2 mg/mL) two hours after the first modeling each day. Mice in the control group and the model group were applied with an equal volume of pure water; once a day, until the end of the modeling process. After last medication, skin lesions and pathological morphology of the mice were observed. Immunofluorescence was used to detect the expressions of Filaggrin, Loricrin and Ki67 proteins in skin tissue of the mice. The core pathways through which
D. officinale
improves skin damage in xeroderma were screened using 16S rRNA sequencing combined with gene ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses, and subsequent validation was conducted.
RESULTS
2
Compared with the control group, the mice in the model group exhibited obvious scratching behavior, with a large amount of scale on the skin, excessive epidermal keratinization, and thickened stratum spinosum. The skin scale score, epidermal thickness, and the expression levels of Ki67, Filaggrin, and Loricrin proteins in the skin tissue were significantly increased/elevated (
P
<0.05). Compared with model group, the mice in the
D. officinale
group exhibited reduced scratching behavior and scaling, along with a mitigated degree of skin keratinization. The aforementioned quantitative indicators were significantly decreased/reduced (
P
<0.05). The results of core pathway screening revealed that the KEGG pathways involving differentially expressed genes included signaling pathways such as interleukin-17 (IL-17) and tumor necrosis factor (TNF). Further validation experim
ents found that after intervention with
D. officinale
, mRNA expression of downstream effector molecules CCN1, Hbegf, Tnfrsf12a, and Thbs1 genes in skin tissues were all significantly reduced (
P
<0.05).
CONCLUSIONS
2
D. officinale
can repair skin damage in mice with xeroderma, and its mechanism of action is related to restoring the balance of proliferation and differentiation in keratinocytes and down-regulating the mRNA expressions of CCN1, Hbegf, Tnfrsf12a, and Thbs1.
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