The bacterial keratitis causes viability loss and apoptosis in the corneal epithelial cells (CECs). The cyanidin-3-O-glucoside (C3G) benefits visual system and also possess anti-bacterial and anti-inflammatory potentials. In the current study, the effects of C3G on human CECs (HCECs) against bacterial lipopolysaccharide (LPS)-induced disorders were assessed, and the mechanism driving the protective effect was explored by focusing on let-7b-5p-mediated HMGA2/PI3K/Akt pathway. The HCECs were incubated LPS of P. aeruginosa to induce inflammation and apoptosis, and then treated with C3G. The changes in cell viability, apoptosis, and inflammation were detected. Moreover, the effects of LPS and C3G on let-7b-5p level and HMGA2/PI3K/Akt pathway activity were also assessed. Thereafter, the HCECs were further transfected with let-7b-5p inhibitor to confirm its role in the vision-protective effects of C3G. The interaction between let-7b-5p and HMGA2 was verified with dual luciferase assay. The LPS treatment suppressed viability and induced apoptosis and inflammation in HCECs, which was associated with the down-regulated let-7b-5p level and up-regulated HMGA2/PI3K/Akt pathway activity. The impairments of LPS on HCECs were attenuated by C3G: the compound increased cell viability and inhibited apoptosis and inflammation. The C3G also induced let-7b-5p level and inactivated HMGA2/PI3K/Akt pathway. However, after the inhibition of let-7b-5p, the protective effects of C3G on HCECs against LPS were blocked. The results of dual luciferase assay showed the direct binding let-7b-5p to the promoter of HMGA2 gene. It was inferred that the C3G could ameliorate the LPS-induced disorders in HCECs. The effect depended on the induced level of let-7b-5p, which then inhibited HMGA2/PI3K/Akt pathway.

细菌性角膜炎导致角膜上皮细胞（CEC）的活力丧失和凋亡。花青素3-O-葡萄糖苷（C3G）有益于视觉系统，还具有抗菌和消炎的潜力。在本研究中，评估了C3G对人类CEC（HCEC）抵抗细菌脂多糖（LPS）诱导的疾病的作用，并着重于let-7b-5p介导的HMGA2 / PI3K /探索了保护作用的机制。 Akt途径。HCEC是铜绿假单胞菌的LPS孵育诱导炎症和凋亡，然后用C3G治疗。检测到细胞活力，凋亡和炎症的变化。此外，还评估了LPS和C3G对let-7b-5p水平和HMGA2 / PI3K / Akt途径活性的影响。此后，用let-7b-5p抑制剂进一步转染HCEC，以确认其在C3G视力保护作用中的作用。用双重荧光素酶测定法验证了let-7b-5p和HMGA2之间的相互作用。LPS处理抑制HCEC的活力并诱导其凋亡和炎症，这与下调let-7b-5p水平和上调HMGA2 / PI3K / Akt通路活性有关。C3G可减轻HCEC上LPS的损伤：该化合物增加细胞活力并抑制细胞凋亡和炎症。C3G还诱导let-7b-5p水平并使HMGA2 / PI3K / Akt通路失活。但是，在let-7b-5p抑制后，C3G对HCEC抵抗LPS的保护作用被阻断。双重荧光素酶分析的结果表明let-7b-5p与HMGA2基因的启动子直接结合。据推测，C3G可以改善HCEC中LPS诱导的疾病。该作用取决于let-7b-5p的诱导水平，该水平随后抑制了HMGA2 / PI3K / Akt途径。