2022年3月1日 · 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.

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 pulm …

2020年5月1日 · Ruscogenin attenuates lipopolysaccharide-induced pulmonary endothelial apoptosis by suppressing TLR4/MYD88/NF-κB signaling. TLR4 plays a key role in the pathological process of acute lung injury and may be the target protein of ruscogenin.

After LPS treatment of mice via intratracheal instillation (5 mg/kg) for 4 h, EBA dye (50 mg/kg) was administered via tail vein injection. After 2 h, mice were anesthetized and perfused with saline through the right ventricle for 5 min. Mouse lungs were excised, homogenized in 1 mL phosphate buffer solution (PBS), and extracted in 2 mL ...

Erratum: Author correction to 'Ruscogenin alleviates LPS-triggered pulmonary endothelial barrier dysfunction through targeting NMMHC IIA to modulate TLR4 signaling' [Acta Pharmaceutica Sinica B 12 (2022) 1198-1212]

Here we reported that ruscogenin (RUS), an effective steroidal sapogenin of Radix Ophiopogon japonicus, attenuated lipopolysaccha-rides (LPS)-induced pulmonary endothelial barrier disruption through mediating non-muscle myosin heavy chain IIA (NMMHC IIA)‒Toll-like receptor 4 …

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The results showed that RUS could attenuate LPS-induced lung injury and pulmonary endothelial apoptosis significantly. And we observed that RUS inhibited the activation of TLR4/MYD88/NF-κB pathway in pulmonary endothelium after LPS treatment.

2022年7月1日 · Author correction to ‘Ruscogenin alleviates LPS-triggered pulmonary endothelial barrier dysfunction through targeting NMMHC IIA to modulate TLR4 signaling’ [Acta Pharmaceutica Sinica B 12 (2022) 1198–1212]