Results indicated that propofol alleviated LPS-mediated cell damage through GJ function inhibition in vitro and protected against AOLT-induced ALI also through down-regulating Cx43 GJ function, mechanisms of which were both relative with inflammatory reaction modulation, such as TNF-α, IL-1β, IL-6 and IL-8. The gene discussed is GJA1; the disease is acute respiratory distress syndrome.