Objective To explore the ABO blood group and Rh blood group system antigen distribution in Huainan area.Methods To investigate the Huainan area of 24 035 voluntary blood donors of the ABO and Rh blood group system phenotype and gene frequency distribution by the population genetics of the blood type.Results In the Huainan area population,the gene frequency of ABO blood type distribution was r ＞ P ＞ q,the distribution of phenotype was O ＞ A ＞ B ＞ AB,the distribution of RhD(-)frequency was 0.36％,and this result was consistent with the RhD(-)frequency of 0.2％～0.5％ of the Han population in the country.Conclusion ABO blood group and Rh blood group were two separate systems,control their distributed rule in the Huainan region was very important to the clinical use of blood,establishment of a repository of rare blood group of RhD(-),alleviation the lack of state hospital transfusion,raising the level of clinical treatment and to the reducing the incidence of immunological transfusion reactions.

[This corrects the article DOI: 10.1016/j.apsb.2021.09.017.].

Pulmonary endothelial barrier dysfunction is a hallmark of clinical pulmonary edema and contributes to the development of acute lung injury (ALI). Here we reported that ruscogenin (RUS), an effective steroidal sapogenin of Radix Ophiopogon japonicus, attenuated lipopolysaccharides (LPS)-induced pulmonary endothelial barrier disruption through mediating non-muscle myosin heavy chain IIA (NMMHC IIA)‒Toll-like receptor 4 (TLR4) interactions. By in vivo and in vitro experiments, we observed that RUS administration significantly ameliorated LPS-triggered pulmonary endothelial barrier dysfunction and ALI. Moreover, we identified that RUS directly targeted NMMHC IIA on its N-terminal and head domain by serial affinity chromatography, molecular docking, biolayer interferometry, and microscale thermophoresis analyses. Downregulation of endothelial NMMHC IIA expression in vivo and in vitro abolished the protective effect of RUS. It was also observed that NMMHC IIA was dissociated from TLR4 and then activating TLR4 downstream Src/vascular endothelial cadherin (VE-cadherin) signaling in pulmonary vascular endothelial cells after LPS treatment, which could be restored by RUS. Collectively, these findings provide pharmacological evidence showing that RUS attenuates LPS-induced pulmonary endothelial barrier dysfunction by inhibiting TLR4/Src/VE-cadherin pathway through targeting NMMHC IIA and mediating NMMHC IIA‒TLR4 interactions.