Retinal detachment (RD) is a severe sight-threatening complication that can be caused by a multitude of retinal diseases. It has been evidenced that minocycline exerts neuroprotective effects by targeting microglia in the pathogenesis of massive ocular lesions including RD, but mechanisms remain elusive. We carried out this research to elucidate the potential mediators that link RD-induced vision loss with microglia reactivity by discussing effects of minocycline on cytokine levels and A20, a negative regulator of inflammation. Minocycline or vehicle was intraperitoneally administrated immediately after RD and continued daily before animals being euthanized. The oxygen glucose deprivation assay was undertaken on the co-cultured BV-2 and 661W cells to mimic the condition of RD in vitro, where A20 siRNA was adopted to knock down the A20 expression in BV-2 cells. Photoreceptor cells apoptosis, inflammatory response and microglia activity following RD with or without minocycline were evaluated. Photoreceptor cells apoptosis and inflammatory response were induced after RD, which could be largely counteracted by minocycline. Minocycline postponed the migration and proliferation of microglia and facilitated their transition to the M2 subtype following RD. Blocking A20 expression in BV-2 cells with siRNA crippled the effect of minocycline. Collectively, minocycline yields a promoting effect on photoreceptor cells survival post-RD by modulating the transformation of microglia phenotypes, in which process A20 may play a “bridge” role.

视网膜脱离（RD）是一种严重的威胁视力的并发症，可能由多种视网膜疾病引起。已经证明，米诺环素通过靶向小胶质细胞在包括RD在内的大量眼部病变的发病机理中发挥神经保护作用，但机制尚不清楚。我们进行了这项研究，以通过讨论米诺环素对细胞因子水平和炎症负调节剂A20的影响，阐明将RD引起的视力丧失与小胶质细胞反应性联系起来的潜在介体。RD后立即腹膜内施用米诺环素或媒介物，并在对动物实施安乐死之前每天持续进行。在共培养的BV-2和661W细胞上进行了氧葡萄糖剥夺试验，以模拟RD的体外条件，其中采用A20 siRNA敲低BV-2细胞中A20的表达。评估在有或没有米诺环素的情况下，RD后的感光细胞凋亡，炎症反应和小胶质细胞活性。RD后诱导了感光细胞的凋亡和炎症反应，这可能被美满霉素所抵消。米诺环素推迟了小胶质细胞的迁移和增殖，并促进了它们在RD后向M2亚型的过渡。用siRNA阻断BV-2细胞中A20的表达削弱了米诺环素的作用。总而言之，米诺环素通过调节小胶质细胞表型的转化而对RD后的感光细胞存活产生促进作用，在该过程中A20可能起着“桥梁”的作用。在有或没有米诺环素的情况下，评估了RD后的炎症反应和小胶质细胞活性。RD后诱导了感光细胞的凋亡和炎症反应，这可能被美满霉素所抵消。米诺环素推迟了小胶质细胞的迁移和增殖，并促进了它们在RD后向M2亚型的过渡。用siRNA阻断BV-2细胞中A20的表达削弱了米诺环素的作用。总而言之，米诺环素通过调节小胶质细胞表型的转化而对RD后的感光细胞存活产生促进作用，在该过程中A20可能起着“桥梁”的作用。在有或没有米诺环素的情况下，评估了RD后的炎症反应和小胶质细胞活性。RD后诱导了感光细胞的凋亡和炎症反应，这可能被美满霉素所抵消。米诺环素推迟了小胶质细胞的迁移和增殖，并促进了它们在RD后向M2亚型的过渡。用siRNA阻断BV-2细胞中A20的表达削弱了米诺环素的作用。总而言之，米诺环素通过调节小胶质细胞表型的转化而对RD后的感光细胞存活产生促进作用，在该过程中A20可能起着“桥梁”的作用。米诺环素推迟了小胶质细胞的迁移和增殖，并促进了它们在RD后向M2亚型的过渡。用siRNA阻断BV-2细胞中A20的表达削弱了米诺环素的作用。总而言之，米诺环素通过调节小胶质细胞表型的转化而对RD后的感光细胞存活产生促进作用，在该过程中A20可能起着“桥梁”的作用。米诺环素推迟了小胶质细胞的迁移和增殖，并促进了它们在RD后向M2亚型的过渡。用siRNA阻断BV-2细胞中A20的表达削弱了米诺环素的作用。总而言之，米诺环素通过调节小胶质细胞表型的转化而对RD后的感光细胞存活产生促进作用，在该过程中A20可能起着“桥梁”的作用。