Inflammation and apoptosis of chondrocytes are the pathological bases of osteoarthritis. Autophagy could alleviate the symptoms of inflammation and apoptosis. Previous study has shown that BCL2/adenovirus E1B 19 kDa protein-interacting protein 3 (BNIP3) can induce the occurrence and development of autophagy. However, it is unknown whether autophagy induced by BNIP3 can alleviate the inflammation and apoptosis of chondrocytes. We used the lentivirus to construct the overexpression BNIP3 chondrocytes. Next, the lipopolysaccharide (LPS) was used to stimulate these cells to simulate the physiological environment of osteoarthritis. After that, the enzyme-linked immunosorbent assays (ELISA) were performed to determine the levels of tumor necrosis factor-α (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6) and the flow cytometry was performed to detect the apoptosis rates of chondrocytes. At last, the expression of autophagy-related proteins was detected with the western blotting. The expression of BNIP3 was suppressed after treatment with LPS. However, overexpression of BNIP3 inhibited the secretion of proinflammatory factors (TNF-α, IL-1β, and IL-6) and decreased the apoptosis of chondrocytes. Furthermore, overexpression of BNIP3 led to the upregulation of autophagy-related protein expression including little computer 3 (LC3), autophagy-related protein 7 (ATG7), and Beclin-1. Application of autophagy inhibitor recovered the expression of proinflammatory factors and apoptosis rates of chondrocytes. BNIP3 decreased the LPS-induced inflammation and apoptosis of chondrocytes by activating the autophagy.

中文翻译：

---

BNIP3通过促进自噬的发展来减少LPS诱导的软骨细胞炎症和凋亡。

软骨细胞的炎症和凋亡是骨关节炎的病理基础。自噬可以减轻炎症和细胞凋亡的症状。先前的研究表明，BCL2 /腺病毒E1B 19 kDa蛋白相互作用蛋白3（BNIP3）可以诱导自噬的发生和发展。然而，尚不清楚由BNIP3诱导的自噬能否减轻软骨细胞的炎症和凋亡。我们使用慢病毒来构建过表达的BNIP3软骨细胞。接下来，使用脂多糖（LPS）刺激这些细胞以模拟骨关节炎的生理环境。之后，进行酶联免疫吸附测定（ELISA），以确定肿瘤坏死因子-α（TNF-α），白介素-1β（IL-1β），白细胞介素6（IL-6）和流式细胞仪检测软骨细胞的凋亡率。最后，通过western blotting检测自噬相关蛋白的表达。用LPS处理后，BNIP3的表达被抑制。然而，BNIP3的过表达抑制促炎因子（TNF-α，IL-1β和IL-6）的分泌，并降低软骨细胞的凋亡。此外，BNIP3的过表达导致自噬相关蛋白表达上调，包括小计算机3（LC3），自噬相关蛋白7（ATG7）和Beclin-1。自噬抑制剂的应用恢复了促炎因子的表达和软骨细胞的凋亡率。BNIP3通过激活自噬减少了LPS诱导的软骨细胞炎症和凋亡。