We has been committed to explore the pathogenesis, latest prevention and treatment methods of sepsis-induced ARDS. In recent 5 years, we have published more than 10 papers related to ARDS. Our research group found that patients with cervical spinal cord injury accompanied by sympathetic chain damage (typical manifestations of α-AR blockade, such as slow heart rate and low blood pressure) had a lower incidence of ARDS, and began to pay attention to the study of "the relationship between sympathetic nerves and ARDS". And then we found that α2-adrenoceptor specific antagonist yohimbine can reduce the lung tissue pathology injury score, reduce infiltration of inflammatory cells and alleviate lung injury. Subsequently, some scholars found that blocking α2A-adrenoceptor can improve lung injury in septic rats, but the mechanism is unclear. On this basis, we constructed a mouse model of ARDS by endotracheal infusion of LPS, and used α2A-adrenoceptor blocker BRL44408 to intervene. We found that blocking α2A-adrenoceptor alleviated the inflammatory response of lung tissues by inhibiting the activation of ERK and improved lung injury in mice. In the future, we will continue to explore the role of different adrenergic receptors in ARDS and other sepsis-induced organ damage, and further clarify the mechanism.
Research Keywords & Expertise
Sepsis
Spinal Cord Injury
acute lung injury
acute respiratory dist...
Critical Care and Mult...
Short Biography
We has been committed to explore the pathogenesis, latest prevention and treatment methods of sepsis-induced ARDS. In recent 5 years, we have published more than 10 papers related to ARDS. Our research group found that patients with cervical spinal cord injury accompanied by sympathetic chain damage (typical manifestations of α-AR blockade, such as slow heart rate and low blood pressure) had a lower incidence of ARDS, and began to pay attention to the study of "the relationship between sympathetic nerves and ARDS". And then we found that α2-adrenoceptor specific antagonist yohimbine can reduce the lung tissue pathology injury score, reduce infiltration of inflammatory cells and alleviate lung injury. Subsequently, some scholars found that blocking α2A-adrenoceptor can improve lung injury in septic rats, but the mechanism is unclear. On this basis, we constructed a mouse model of ARDS by endotracheal infusion of LPS, and used α2A-adrenoceptor blocker BRL44408 to intervene. We found that blocking α2A-adrenoceptor alleviated the inflammatory response of lung tissues by inhibiting the activation of ERK and improved lung injury in mice. In the future, we will continue to explore the role of different adrenergic receptors in ARDS and other sepsis-induced organ damage, and further clarify the mechanism.