LncRNA SNHG10 对脂多糖诱导血管内皮 细胞氧化应激损伤的影响.

Objective To explore the effect of lncRNA SNHG10 on lipopolysaccharide （LPS)-induced oxidative stress injury in vascular endothelial cells. Methods The optimal concentration of LPS was screened out to be 500 ng/ mL. The in vitro models were constructed by inducing human umbilical vein endothelial cells （HUVEC) with LPS. HU⁃ VEC in the logarithmic growth phase were taken, si-NC and si-SNHG10 plasmids were transfected into HUVEC, and then the cells were treated with LPS （500 ng/mL)（recorded as LPS + si-NC group and LPS+si-SNHG10 group, respectively). HUVEC without any treatment were selected as the Control group, and only 500 ng/mL LPS was added. CCK-8 and flow cytometry were used to detect cell viability and apoptosis level； RT-qPCR was used to detect the relative expression of small nucleolar RNA host gene 10（SNHG10)； Western blotting was used to detect Ki-67, Bcl-2, and Bax； ELISA was used to detect tumor necrosis factor-α（TNF-α), interleukin 6（IL-6), interleukin 1β（IL-1β), MDA content, and SOD activity. Results The cell viability, Ki-67 protein, and Bcl-2 protein expression of HUVEC in the LPS + si-SNHG10 group were 75. 6% ± 4. 1%, 0. 74 ± 0. 06, 0. 65 ± 0. 05, and they were 45. 4 ± 2. 8%, 0. 52% ± 0. 04, and 0. 42 ± 0. 03, respectively, in the LPS+si-NC group； SNHG10 expression, apoptosis rate, Bax protein expression, TNF-α, 1L-6 and 1L-1β expression in the LPS+si-SNHG10 group were 1. 88 ± 0. 11, 16. 8% ± 0. 9%, 1. 32 ± 0. 07(289. 2 ± 25. 1) pg/mL(363. 3 ± 22. 4) pg/mL, and （402. 6 ± 21. 3) pg/mL, which were 3. 24 ± 0. 19, 23. 1% ± 1. 2%, 1. 68 ± 0. 11(536. 6 ± 33. 0) pg/mL(634. 5 ± 33. 1) pg/mL, and （664. 5 ± 38. 1) pg/mL, respectively, in the LPS + si-NC group. SNHG10 expression, apoptosis rate, Bax protein expression, TNF-α, 1L-6, and 1L-1β expression levels were lower in the LPS + si-SNHG10 group than in the LPS + si-NC group （all P<0. 05). Compared with the Control group, the expression of MDA increased in the LPS group （P<0. 05), and the SOD activity decreased （P<0. 05)； compared with the LPS + si-NC group, MDA in HUVEC cells of the LPS + si-SNHG10 group decreased （P<0. 05), while the SOD activity increased （P< 0. 05). Conclusion Interfering with the expression of SNHG10 can alleviate the apoptosis, inflammation and oxidative stress of LPS-induced HUVEC, and promote cell proliferation. [ABSTRACT FROM AUTHOR]