动物皮脂质

TER-C14产生低皮肤刺激，且仅衍生物降低皮肤脂质有序性，但皮肤脂质本身并非刺激原。

TER-C14 showed low skin irritation; derivatives decreased order of skin lipids, but skin lipids themselves are not irritants.

研究显示SPPs对皮肤脂质屏障无影响（电阻、TEWL、FTIR无变化），且皮肤刺激性和细胞毒性可忽略。

SPPs did not alter skin lipid barrier (no change in resistance, TEWL, FTIR) and showed negligible skin irritation and cytotoxicity.

酯类增强剂几乎无皮肤刺激和细胞毒性，且仅酯类能降低皮肤脂质有序性，但皮肤脂质本身并非刺激原。

The esters showed almost no skin irritation and cytotoxicity; they decreased order of skin lipids, but skin lipids themselves are not irritants.

皮肤拭子物质（SSS）破坏泪膜完整性，引起刺痛和角膜上皮损伤，证实皮肤脂质有眼刺激风险。

Skin swab substances (SSS) disrupted tear film integrity, caused stinging and corneal epithelial damage, confirming eye irritation risk of skin lipids.

皮肤脂质中的9-DDHC在UVA照射下产生ROS，导致角质形成细胞活力下降，证实皮肤脂质具有光毒性

9-DDHC in skin lipids generates ROS upon UVA irradiation, reducing keratinocyte viability, confirming phototoxicity of skin lipids

蚯蚓光毒性反应与皮肤脂质中的光活性甾醇相关，且人体皮肤中存在类似甾醇，提示皮肤脂质具有光毒性风险

Phototoxic response in earthworms is related to photoactive sterols in skin lipids, and similar sterols are found in human skin, indicating phototoxicity risk of skin lipids

综述讨论皮脂与痤疮关系，提出皮脂中低亚油酸水平导致毛囊角化过度和粉刺形成，但未提供具体实验数据或测试浓度，仅机理推测。

Review discusses sebum-acne relationship, proposing low linoleate in sebum leads to follicular hyperkeratosis and comedo formation, but no experimental data or concentration provided, only mechanistic speculation.

皮肤脂质作为模型，乙醇提取皮肤脂质（FFA）并增强渗透，但皮肤脂质本身是被动靶标，未证实其自身有经皮渗透风险。

Skin lipids are model; ethanol extracts skin lipids (FFA) and enhances permeation, but skin lipids themselves are passive target, not confirmed to have percutaneous penetration risk.

皮肤脂质作为屏障，HA与皮肤脂质相互作用导致脂质排列更无序，但未证实皮肤脂质本身有经皮渗透风险；HA作为增强剂，皮肤脂质是被动成分。

Skin lipids act as barrier; HA interacts with skin lipids causing disorder, but does not confirm percutaneous penetration risk of skin lipids themselves; HA is enhancer, skin lipids are passive component.

皮肤脂质作为屏障，肽未改变皮肤脂质屏障（电阻、TEWL、FTIR），皮肤脂质未表现出经皮渗透风险。

Skin lipids act as barrier; peptides did not alter skin lipid barrier (resistance, TEWL, FTIR); skin lipids did not show percutaneous penetration risk.

皮肤脂质在水合下形成池，但水合增强大分子渗透，皮肤脂质本身未表现出经皮渗透风险；水合是可逆的，未永久损伤。

Skin lipids form cisternae under hydration, but hydration enhances macromolecule penetration; skin lipids themselves do not show percutaneous penetration risk; hydration is reversible without permanent damage.

研究脂质体组成对渗透的影响，皮肤脂质作为脂质体成分之一，但未单独评估其经皮渗透风险；结论是脂质体渗透与流动性相关，未证实皮肤脂质本身有风险。

The study investigates liposome composition effects on penetration; skin lipids are a component of liposomes but not evaluated alone for percutaneous penetration risk; conclusion relates liposome fluidity to penetration, not confirming risk of skin lipids.

皮肤脂质（SCLL）作为对照，未显示增强渗透；脂质体本身未渗透到颗粒层，但含DOPE的脂质体可渗透更深，皮肤脂质作为成分未表现出经皮渗透风险。

Skin lipids (SCLL) were used as control and did not enhance penetration; liposomes themselves did not penetrate into granular layers, but DOPE-containing liposomes penetrated deeper; skin lipids as ingredient did not show percutaneous penetration risk.

皮肤脂质（神经酰胺）被脂质分散系统提取减少，但皮肤脂质本身作为成分未表现出经皮渗透风险；研究的是脂质分散系统的增强作用，皮肤脂质是被动靶标。

Skin lipids (ceramides) are extracted and decreased by lipid disperse system, but skin lipids themselves as ingredient do not show percutaneous penetration risk; study focuses on enhancement effect of LDS, skin lipids are passive target.