Introduction Limited by the specific location of atopic facial dermatitis, treatment options for atopic dermatitis are limited. Our previous research confirms that BiShengZhiYan cream (BSZY cream) can reconstruct the damaged skin barrier and strengthen the repair ability of skin. However, little evidence of its efficacy and safety for the treatment of atopic facial dermatitis is available. Methods and analysis A protocol for a randomised, double-blind, controlled trial of BSZY cream is designed for patients with mild-to-moderate atopic facial dermatitis. We will recruit 130 patients with mild-to-moderate atopic facial dermatitis from the Yueyang Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine. The participants will be assigned to the BSZY cream group (treatment group) or the emulsion matrix group (control group) randomly. The intervention period will be 4 weeks, once daily in the morning and once in the evening. The primary outcome is the Scoring Atopic Dermatitis Scale. The Clinical Dermatologist Evaluation Form, Patient Self-Assessment Questionnaire and Safety Indicators will be evaluated as secondary outcomes. The follow-up will be conducted at week 8±3 days. The skin condition is assessed by a clinical dermatologist at week 0±3 days, week 2±3 days and week 4±3 days. Ethics and dissemination The protocol has been approved by Shanghai University of Traditional Chinese Medicine’s Yueyang Hospital ethics committee (No. 2023-024). All participants will be asked to sign an informed consent in compliance with the Declaration of Helsinki. On completion of the trial, we plan to disseminate the results through peer-reviewed publications and present the findings at relevant scientific conferences. Data will be provided on reasonable request under participant confidentiality and data privacy regulations. Trial registration number NCT05792826.

Endothelial cells under oxidative stress and inflammation are vital contributors to the progression of atherosclerosis. Although Orientin possesses antioxidant and anti‐inflammatory activities, the effects of Orientin on oxidized low‐density lipoprotein and high glucose (ox‐LDL/HG)–triggered endothelial cell injury and diabetes‐accelerated atherosclerosis remain unclear. ApoE ^−/− mice were administered streptozotocin (STZ), fed with high‐fat diet (HFD), and then treated with Orientin to test the efficacy of Orientin on ameliorating atherosclerosis through pathological and biochemical assays. Human aortic endothelial cells (HAECs) were stimulated by ox‐LDL/HG followed by Orientin treatment, and the effects of Orientin on regulating HAEC viability, oxidative stress, inflammation, and endothelial‐mesenchymal transition (EndMT) were assessed using cell counting kit‐8 (CCK‐8), fluorescein diacetate (FDA) staining, quantitative real‐time PCR, immunofluorescence (IF), and western blot assays. The results showed that Orientin treatment decreased atherosclerotic plaque burden, lipid lesion, and collagen content in aortic and femoral arteries in diabetic mice. Meanwhile, Orientin alleviated hypercholesterolemia, as evidenced by decreased levels of total cholesterol, LDL‐cholesterol, and triglyceride. In HAECs, Orientin treatment increased cell viability and decreased inflammation, oxidative stress, and EndMT induced by ox‐LDL/HG. Furthermore, Orientin significantly inhibited reactive oxygen species (ROS)–triggered NOD‐like receptor family pyrin domain containing 3 (NLRP3) inflammasome activation and pyroptosis, as suggested by cleavage of caspase‐1 and gasdermin‐D (GSDMD), generation of interleukin (IL)‐18 and IL‐1β, and lactate dehydrogenase (LDH) release. Mechanistically, Orientin increased E3 ubiquitin ligase membrane‐associated RING‐CH 8 (MARCH8) expression in HAECs and resulted in subsequent MARCH8‐mediated ubiquitination and proteasomal degradation of the NLRP3 protein. Taken together, these data demonstrate that Orientin, which alleviates HAEC inflammation and pyroptosis through regulating the MARCH8/NLRP3 axis, might be a potential candidate for treating diabetes‐accelerated atherosclerosis.