Effects of P1G10 against UVB-induced damage: Reduction of antioxidant stress, inflammation and cell proliferation

IF 3.261
Kátia M. Freitas , Emerson S. Veloso , Ênio Ferreira , Marcelo V. Caliari , Carlos E. Salas , Miriam T.P. Lopes
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引用次数: 0

Abstract

Background

P1G10 is the proteolytic fraction from Vasconcellea cundinamarcensis latex equivalent to papain from C. papaya. It acts as healing enhancer in diverse wound scenarios. In a preliminary study P1G10 showed promising anti-inflammatory activity in lesions induced by single dose UVB irradiation.

Aim

The present study assesses the impact of P1G10 topically applied on mice lesions induced by multiple UVB doses.

Results

After repeated exposure to 240 mJ cm-2 UVB, P1G10 decreased by ∼50 % the detected ROS, enhanced glutathione peroxidase (GPx) and catalase activities, thereby protecting against oxidative stress. The anti-inflammatory effect of the fraction was consolidated by reduction in TNF-α (∼70 %) and IL1β (∼90 %) and confirmed by histological analyses showing a reduction in cellularity and leukocyte infiltration into the hypodermis. Additionally, epidermal hyperplasia induced by UVB was reduced as shown by a decrease of PCNA immunolabeling in keratinocytes. Pathways involved in the inflammatory process and in UVB-induced production of free radicals were also affected, revealing that P1G10 application reduced phosphorylation of MAP kinase proteins (JNK and P38) and Akt, as well as MMP-9 activity.

Conclusions

These data confirm the lasting protective action of P1G10 by moderating oxidative stress and apoptosis induced by multiple doses of UV-B in the skin, suggesting a potential preventive action against the onset of carcinogenesis.

Abstract Image

P1G10抗uvb损伤的作用:减少抗氧化应激、炎症和细胞增殖
背景:p1g10是Vasconcellea cundinamarcensis乳胶的蛋白水解部分,相当于C. papaya的木瓜蛋白酶。它在不同的伤口情况下起到愈合促进剂的作用。在初步研究中,P1G10在单剂量UVB照射引起的病变中显示出良好的抗炎活性。目的观察局部应用P1G10对多剂量UVB致小鼠损伤的影响。结果反复暴露于240 mJ cm-2 UVB后,P1G10检测到的ROS减少~ 50%,谷胱甘肽过氧化物酶(GPx)和过氧化氢酶活性增强,从而保护氧化应激。该组分的抗炎作用通过降低TNF-α(~ 70%)和il - 1β(~ 90%)得到巩固,并通过组织学分析证实,显示细胞数量和白细胞浸润到皮下组织的减少。此外,UVB诱导的表皮增生减少,如角质形成细胞中PCNA免疫标记的减少。参与炎症过程和uvb诱导自由基产生的途径也受到影响,表明P1G10的应用降低了MAP激酶蛋白(JNK和P38)和Akt的磷酸化,以及MMP-9的活性。结论P1G10通过调节多剂量UV-B诱导的皮肤氧化应激和细胞凋亡,具有持久的保护作用,提示P1G10具有潜在的预防癌变的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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CiteScore
4.10
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