摘要
牛磺酸通过激活细胞膜上的甘氨酸受体(GlyR)而抑制Kupffer细胞(KC)的活性.GlyR通道的激活促使氯离子内流,导致细胞膜超极化进而抑制脂多糖(LPS)诱导的KC激活.在内毒素诱导的大鼠肝损伤模型中,喂食牛磺酸可通过激活GlyR,继而抑制KC起到保护肝损伤的作用.在高渗透压下,LPS诱导的环氧化酶-2和前列腺素的合成明显增加.牛磺酸可抑制KC内高渗透压诱导的环氧化酶-2和前列腺素,而对LPS诱导的肝损伤起到保护作用.牛磺酸可能有益于LPS诱导的肝损伤的临床治疗.
Taurine has been characterized as an inhibitor of Kupffer cells which activates a glycine recep-tor(GlyR)expressing in cell membranes.Ac-tivation of the GlyR channel allows the influx of chloride,preventing depolarization of the plasma membrane and the potentiation of ex-citatory signals in Kupffer cells.Dietary taurine has protective effects in rat models against li-popolysaccharide(LPS)-induced liver injury by inactivating Kupffer cells via actvivating GlyR.LPS leads to an induction of cyclooxygenase-2 and prostanoid forma tion,which are markedly enhanced during hyperosmotic conditions.It’s been demonstrated that taurine protects against LPS-induced liver injury in Kupffer cells by inhibiting the hyperosmolarity-induced induction of cyclooxygenase-2 and stimulation of prostaglandin production.Taurine may be useful in clinic for the treatment of LPS-induced liver injury.
作者
张耘
魏思东
龚建平
Yun Zhang;Si-Dong Wei;Jian-Ping Gong(Department of General Surgery,the Ninth People’s Hospital of Chongqing Municipality,Chongqing 400700,China;Department of Hepatobiliary Surgery,the Second Affiliated Hospital of Chongqing Medical University,Chongqing 400010,China)
出处
《世界华人消化杂志》
CAS
北大核心
2008年第24期2756-2760,共5页
World Chinese Journal of Digestology
基金
国家自然科学基金资助项目,No.30471969,No.30772098
