Abstract：
BACKGROUND: The aim of this study was to explore the anti-inflammatory and anti-lipid effects of lactoferrin on SZ95 human sebaceous gland cells and mouse model of acne.
METHODS: SZ95 cells were co-cultured with different concentrations of lactoferrin, and cell viability was determined using the 2,5-diphenyl-2H-tetrazolium bromide method. Oil red O and Nile red staining were performed to determine the lipid content. The mRNA expression of genes related to lipid metabolism (sterol regulatory element-binding protein-1 [SREBP-1], fatty acid synthase [FAS], stearoyl-CoA desaturase-1 [SCD-1], fatty acid desaturase 2 [FADS2]) and inflammation (interleukin-8 [IL-8]) was determined by reverse transcription-polymerase chain reaction. An acne mouse model was established using injection of P. acnes on the backs of mice. The proliferation and apoptosis of sebaceous gland cells were examined by immunohistochemistry against proliferating cell nuclear antigen (PCNA) and TUNEL staining, respectively. Western blotting was used to detect FADS2 and CXCL15 protein expression.
RESULTS: Lactoferrin treatment at 10-500 μg/ml significantly decreased the lipid content, as revealed by the oil red O and Nile red staining. It also attenuated the increase of mRNA expression of SREBP-1, FAS, SCD-1, FADS2, and IL-8 in insulin-treated SZ95 cells. Moreover, lactoferrin treatment at the doses of 1-50 mg/mouse significantly reduced the inflammation and lipid production in the mouse model of acne. Also, the number of sebaceous gland cells was significantly reduced, and apoptosis was significantly increased by lactoferrin treatment in the mice. Mechanically, the levels of FADS2 and CXCL15 proteins in tissues were significantly decreased after lactoferrin treatment in the model mice.
CONCLUSIONS: Our results demonstrate the potential of lactoferrin against sebogenesis, sebaceous gland inflammation in acne.
METHODS: SZ95 cells were co-cultured with different concentrations of lactoferrin, and cell viability was determined using the 2,5-diphenyl-2H-tetrazolium bromide method. Oil red O and Nile red staining were performed to determine the lipid content. The mRNA expression of genes related to lipid metabolism (sterol regulatory element-binding protein-1 [SREBP-1], fatty acid synthase [FAS], stearoyl-CoA desaturase-1 [SCD-1], fatty acid desaturase 2 [FADS2]) and inflammation (interleukin-8 [IL-8]) was determined by reverse transcription-polymerase chain reaction. An acne mouse model was established using injection of P. acnes on the backs of mice. The proliferation and apoptosis of sebaceous gland cells were examined by immunohistochemistry against proliferating cell nuclear antigen (PCNA) and TUNEL staining, respectively. Western blotting was used to detect FADS2 and CXCL15 protein expression.
RESULTS: Lactoferrin treatment at 10-500 μg/ml significantly decreased the lipid content, as revealed by the oil red O and Nile red staining. It also attenuated the increase of mRNA expression of SREBP-1, FAS, SCD-1, FADS2, and IL-8 in insulin-treated SZ95 cells. Moreover, lactoferrin treatment at the doses of 1-50 mg/mouse significantly reduced the inflammation and lipid production in the mouse model of acne. Also, the number of sebaceous gland cells was significantly reduced, and apoptosis was significantly increased by lactoferrin treatment in the mice. Mechanically, the levels of FADS2 and CXCL15 proteins in tissues were significantly decreased after lactoferrin treatment in the model mice.
CONCLUSIONS: Our results demonstrate the potential of lactoferrin against sebogenesis, sebaceous gland inflammation in acne.
摘要：
背景：本研究的目的是探讨乳铁蛋白对SZ95人皮脂腺细胞和痤疮小鼠模型的抗炎和抗脂作用。
方法：将SZ95细胞与不同浓度的乳铁蛋白共培养，并使用2,5-二苯基-2H-四唑溴化物法测定细胞活力。进行油红O和尼罗红染色以确定脂质含量。与脂质代谢相关的基因的mRNA表达（固醇调节元件结合蛋白-1[SREBP-1]，脂肪酸合成酶[FAS]，硬脂酰辅酶A去饱和酶-1[SCD-1]，脂肪酸去饱和酶2[FADS2]）和炎症（白介素8[IL-8]）通过逆转录聚合酶链反应确定。使用在小鼠背部注射痤疮丙酸杆菌来建立痤疮小鼠模型。通过针对增殖细胞核抗原（PCNA）的免疫组织化学和TUNEL染色检查皮脂腺细胞的增殖和凋亡。分别。Western印迹法检测FADS2和CXCL15蛋白表达。
结果：乳铁蛋白以10-500μg/ml处理可显著降低脂质含量，如油红O和尼罗河红染色所示。它还减弱了SREBP-1，FAS，胰岛素处理的SZ95细胞中的SCD-1、FADS2和IL-8。此外，1-50mg/小鼠剂量的乳铁蛋白治疗可显着降低痤疮小鼠模型的炎症和脂质产生。此外，皮脂腺细胞数量显著减少,乳铁蛋白治疗小鼠细胞凋亡明显增加。机械上,模型小鼠乳铁蛋白处理后,组织中FADS2和CXCL15蛋白水平显著降低。
结论：我们的结果证明了乳铁蛋白对抗皮脂生成的潜力，皮脂腺炎症在痤疮。
方法：将SZ95细胞与不同浓度的乳铁蛋白共培养，并使用2,5-二苯基-2H-四唑溴化物法测定细胞活力。进行油红O和尼罗红染色以确定脂质含量。与脂质代谢相关的基因的mRNA表达（固醇调节元件结合蛋白-1[SREBP-1]，脂肪酸合成酶[FAS]，硬脂酰辅酶A去饱和酶-1[SCD-1]，脂肪酸去饱和酶2[FADS2]）和炎症（白介素8[IL-8]）通过逆转录聚合酶链反应确定。使用在小鼠背部注射痤疮丙酸杆菌来建立痤疮小鼠模型。通过针对增殖细胞核抗原（PCNA）的免疫组织化学和TUNEL染色检查皮脂腺细胞的增殖和凋亡。分别。Western印迹法检测FADS2和CXCL15蛋白表达。
结果：乳铁蛋白以10-500μg/ml处理可显著降低脂质含量，如油红O和尼罗河红染色所示。它还减弱了SREBP-1，FAS，胰岛素处理的SZ95细胞中的SCD-1、FADS2和IL-8。此外，1-50mg/小鼠剂量的乳铁蛋白治疗可显着降低痤疮小鼠模型的炎症和脂质产生。此外，皮脂腺细胞数量显著减少,乳铁蛋白治疗小鼠细胞凋亡明显增加。机械上,模型小鼠乳铁蛋白处理后,组织中FADS2和CXCL15蛋白水平显著降低。
结论：我们的结果证明了乳铁蛋白对抗皮脂生成的潜力，皮脂腺炎症在痤疮。
