The skin photoprotective effect of trilinolein: Induction of cellular autophagy via the AMPK-mTOR signaling pathway.

Trilinolein (TL) is an active substance contained in traditional Chinese herbs; modern studies have shown that trilinolein has anti-inflammatory and antioxidant effects on the body. This study delves into the photoprotective effect of trilinolein on UVB-irradiated Human Skin Fibroblast (HSF) cells and the underlying mechanisms. Our findings reveal that trilinolein had a photoprotective effect on HSF cells: trilinolein enhanced cellular autophagy, restored UVB-inhibited cell proliferative viability, and curbing UVB-induced reactive oxygen species (ROS) and apoptosis. Intriguingly, after inhibition of TL-induced autophagy via wortmannin, diminished trilinolein's photoprotective effects. Meanwhile, trilinolein was shown to modulate the AMPK-mTOR signaling pathway, thus enhance cellular autophagy in HSF cells, and this tendency was suppressed after the administration of compound C (AMPK inhibitor). In a mouse model of skin photodamage, trilinolein significantly mitigated photodamage extent through morphological and histopathological analyses. This study illuminates trilinolein could inhibit the photodamaging effects of UVB irradiation by regulating cellular autophagy through the AMPK-mTOR signaling pathway, suggesting its promising application in combating UV-induced skin disorders.

Effect of lncRNA CDKN2B-AS1 on malignant biological behaviors of melanoma B16-F10 cells / 中国肿瘤生物治疗杂志

@#Objective: To investigate the effect of long non-coding RNA CDKN2B antisense RNA 1 (CDKN2B-AS1) on malignant biological behaviors of melanoma B16-F10 cells by targeting miR-7-5p. Methods: Melanoma B16-F10 cells were chosen for this study. shRNA CDKN2B-AS1 vector was constructed and transfected into B16-F10 cells. The experimental cells were divided into control group, sh-CDKN2B-AS1 group, miR-7-5p mimic group and miR-7-5p inhibitor group. The expression level of CDKN2B-AS1 mRNA in the transfected B16-F10 cells was detected by RT-PCR; the number of clone formation and the proliferation ability of the cells were detected by Clone formation assay and MTT assay; and the migration and invasion ability of the cells were detected by Scratch-healing assay and Transwell assay. The targeting relationship between CDKN2B-AS1 and miR-7-5p was detected by Luciferase reporter gene assay. The mRNA expression of miR-7-5p and protein expressions of Ki67, cleaved caspase-3, E-cadherin, N-cadherin and Twist1 in B16-F10 cells after transfection with miR-7-5p mimics/inhibitor were detected by RT-PCR and Western blotting, respectively. Results: Compared with the control group, the expression level of CDKN2B-AS1 mRNA in B16-F10 cells of sh-CDKN2B-AS1 group was significantly decreased (P<0.01); the proliferation, migration and invasion ability of cells were significantly decreased (all P<0.01). Luciferase reporter gene assay showed that CDKN2B-AS1 directly targeted miR-7-5p. The mRNAexpression of miR-7-5p, and protein expressions of cleaved caspase-3 and E-cadherininsh-CDKN2B-AS1groupandmiR-7-5pmimic group were significantly up-regulated (all P<0.05), whiletheproteinexpressionsofKi67,N-cadherin,andTwist1weresignificantlydown-regulated (all P<0.05). Conclusion: CDKN2B-AS1 targets miR-7-5p to promote the development of melanoma, and interfering with CDKN2B-AS1 can inhibit the malignant biological behaviors of melanoma B16-F10 cells.