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Potential for tyndalized Lactobacillus acidophilus as an effective component in moisturizing skin and anti-wrinkle products

机译:酪氨酸化嗜酸乳杆菌作为保湿皮肤和抗皱产品的有效成分的潜力

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摘要

It is widely accepted that ultraviolet (UV) irradiation induces skin damage. In the present study, a UVB-induced hairless mouse model of skin photoaging was developed to determine whether tyndalized Lactobacillus acidophilus was able to significantly enhance the repair of photodamaged skin. To evaluate the effects of tyndalized L. acidophilus on UVB-induced skin-wrinkle formation in vivo, HR-1 hairless male mice were exposed to UVB radiation and orally administered tyndalized L. acidophilus. Compared with the control group, the UVB irradiation mice displayed a significant increase in transepidermal water loss and a reduction in skin hydration. In mice with UVB-induced photodamage, the effacement of the fine wrinkles by tyndalized L. acidophilus was correlated with dermal collagen synthesis, accompanied by histological changes. Furthermore, western blotting was performed to investigate the protein expression levels of matrix metalloproteinases (MMPs) and mitogen-activated protein kinase. Notably, orally administered tyndalized L. acidophilus reduced the expression levels of MMP-1 and MMP-9. Based upon the aforementioned results, it was determined that tyndalized L. acidophilus effectively inhibited the wrinkle formation induced by UVB irradiation, and that this may be attributed to the downregulation of MMPs. Therefore, tyndalized L. acidophilus may be considered a potential agent for preventing skin photoaging and wrinkle formation.
机译:紫外线(UV)引起皮肤损伤已被广泛接受。在本研究中,开发了UVB诱导的皮肤光老化的无毛小鼠模型,以确定酪氨酸化的嗜酸乳杆菌是否能够显着增强光损伤皮肤的修复。为了评估酪氨酸杆菌嗜酸乳杆菌在体内对UVB诱导的皮肤皱纹形成的影响,将HR-1无毛雄性小鼠暴露于UVB辐射下并口服施用酪氨酸杆菌嗜酸乳杆菌。与对照组相比,UVB照射小鼠的表皮水分流失明显增加,皮肤水合作用减少。在患有UVB诱导的光损伤的小鼠中,tydalized嗜酸乳杆菌对细纹的消失与皮肤胶原蛋白的合成相关,并伴有组织学变化。此外,进行了蛋白质印迹实验以研究基质金属蛋白酶(MMP)和有丝分裂原激活的蛋白激酶的蛋白表达水平。值得注意的是,口服施用的酪氨酸化嗜酸乳杆菌降低了MMP-1和MMP-9的表达水平。根据上述结果,确定了酪氨酸化的嗜酸乳杆菌有效地抑制了由UVB辐射诱导的皱纹形成,并且这可能归因于MMP的下调。因此,tydalalized嗜酸乳杆菌可被认为是预防皮肤光老化和皱纹形成的潜在药物。

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