College of Acupuncture-Moxibustion and Orthopaedics, (, Hubei University of Chinese Medicine, Wuhan 430065, China).
School of Basic Medicine, Hubei University of Chinese Medicine, Wuhan 430065, China), (, Hubei University of Chinese Medicine, Wuhan 430065, China.
Zhen Ci Yan Jiu. 2024 Jun 25;49(6):577-584. doi: 10.13702/j.1000-0607.20230379.
To observe the effect of electroacupuncture (EA) stimulation of "Zusanli"(ST36) and"Xuehai"(SP10) on the angiogenesis of the local injured skin tissue in mice with psoriasis, so as to explore its mechanisms underlying improvement of psoriasis-induced skin lesions.
A total of 24 female BALB/c mice aged 6-8 weeks were randomly divided into control, model and EA groups, with 8 mice in each group. The psoriasis-like skin lesion model was established by application of 5% imiquimod (IMQ) cream to the mice's back skin, 62.5 mg/d, for 7 days after local depilation, and the mice of the control group received local application of an equal amount of petroleum jelly once a day for 7 days. EA stimulation (2 Hz/100 Hz) was applied to ST36 and SP10 for 30 min, once daily for 7 consecutive days. Photos of the topical injured skin at the back were taken every day, and the severity of psoriasis lesions (psoriasis area and severity index ［PASI］) was scaled. Following H.E. staining, the morphological changes in the injured skin tissue were observed with epidermal thickness analyzed, and the Masson staining was used to observe the proportion of collagen fibers in the injured skin tissues. Immunohistochemical method was used to detect the expression of microvascular markers CD31 and vascular endothelial growth factor (VEGF) and the microvascular density (MVD) was calculated. Western blot was used to detect the expression levels of CD31, VEGF proteins and mitogen activated protein kinases (MAPK) signaling pathway related proteins p38, phosphorylated p38 (p-p38), extracellular regulated protein kinases (ERK), p-ERK, c-Jun N-terminal kinase (JNK) and p-JNK in the injured skin tissue.
Compared with the control group, the mice in the model group showed an evident increase in the erythema score, scales score, skin thickening score and PASI score, epidermal thickness, proportion of the collagen fibers, MVD value of CD31 and VEGF, and expression levels of CD31 and VEGF proteins, and p-p38/p38, p-ERK/ERK and p-JNK/JNK ratios in the injured skin tissue (<0.001, <0.01). In contrast to the model group, the EA group had a significant decrease in the levels of all the indexes mentioned above (<0.05, <0.01, <0.001).
EA intervention can improve the psoriasis-like skin lesions induced by IMQ in mice, which may be related with its functions in down-regulating the expression of angiogenic related factors CD31 and VEGF proteins and MAPK signaling pathway related proteins in the topical injured skin tissue.
观察电针对银屑病模型小鼠局部皮损组织中血管生成的影响，探讨其改善银屑病皮损的作用机制。
将 24 只 6-8 周龄雌性 BALB/c 小鼠随机分为对照组、模型组和电针组，每组 8 只。模型组小鼠于背部脱毛后，每日局部涂抹 5%咪喹莫特乳膏 62.5 mg/d，共 7d 建立银屑病样皮损模型；对照组小鼠于相同部位每日涂抹等体积的凡士林 1 次，共 7d。电针组于造模第 1 天开始给予双侧“足三里”（ST36）和“血海”（SP10）电针刺激，频率 2 Hz/100 Hz，连续刺激 30min，每日 1 次，共 7d。每天观察小鼠背部皮损的大体照片，采用银屑病面积和严重程度指数（PASI）对皮损严重程度进行评分。H.E.染色后观察皮损组织形态学改变，测量表皮厚度，Masson 染色观察皮损组织中胶原纤维比例。免疫组化法检测微血管标记物 CD31 和血管内皮生长因子（VEGF）的表达，计算微血管密度（MVD）。Western blot 法检测皮损组织中 CD31、VEGF 蛋白及丝裂原活化蛋白激酶（MAPK）信号通路相关蛋白 p38、磷酸化 p38（p-p38）、细胞外调节蛋白激酶（ERK）、磷酸化 ERK（p-ERK）、c-Jun N-末端激酶（JNK）及磷酸化 JNK（p-JNK）的表达水平。
与对照组相比，模型组小鼠红斑评分、鳞屑评分、皮肤增厚评分和 PASI 评分、表皮厚度、胶原纤维比例、CD31 和 VEGF 的 MVD 值、CD31 和 VEGF 蛋白表达水平及皮损组织中 p-p38/p38、p-ERK/ERK 和 p-JNK/JNK 比值均显著升高（<0.001，<0.01）。与模型组相比，电针组上述各指标均显著降低（<0.05，<0.01，<0.001）。
电针干预可以改善咪喹莫特诱导的银屑病样皮损小鼠模型的皮损，其作用机制可能与下调皮损组织中血管生成相关因子 CD31 和 VEGF 蛋白及 MAPK 信号通路相关蛋白的表达有关。
