As a receptor mediating the transmembrane signal transduction in the innate immunity, Toll-like receptor 4 (TLR4) is a bridge between innate immunity and required immunity, and plays an important role when signal-transducing of some cells are activated. Recent reports show that TLR4 expresses in the different glial cells and strongly links to the innate immune activation and inflammatory response in the central nervous system (CNS). TLR4 plays a key role in the processes of brain damage by infection of the CNS, stroke, cerebral hemorrhage and trauma. In this review, we concentrate on recent findings regarding the progress of function and mechanism of TLR4 in the processes of the CNS damage in various diseases.

Objective To explore a method to prepare a model of renal ischemia-reperfusion injury, with mild injury to animals, simple and easy to operate and stable effectiveness. Methods Healthy SD male rats were randomly divided into normal group (group C), sham-operated group (group S) and experimental group (IR group). Rats in the experimental group received a median incision in the middle of the back skin. Through the muscle fascia of each side on the back into the bilateral retroperitoneal space, the bilateral renal pedicles were separated, and closed for 50 min with a mini artery clamp without injury, and then the blood perfusion of the bilateral renal pedicles was resumed by releasing the mini artery clamp. Except that the rats of sham operation group were not blocked the renal pedicle, the rest of the operating steps were consistent with the experimental group. The normal group rats were not treated except for anesthesia. To observe the condition of the rats, serum creatinine (SCr), blood urea nitrogen (BUN) and pathologyical changes in the kidney tissues at 24 h after operating. Results Skin incision was 2. 24 ± 0. 27 cm in the group IR, the right incision of lumbar dorsal fascia and muscle was 1. 36 ± 0. 21 cm, and the left incision was 1. 36 ± 0. 24 cm. The operation time was 3. 30 ± 0. 37 min from incising skin to clamping the bilateral kidney pedicles. The successful rate of model preparation reached 95% in the IR group. Compared with the groups C and S, the levels of SCr and BUN were remarkably increased in the IR group (P ＜0. 01), and renal tubular necrosis scores were also significantly increased (P＜ 0. 05). Conclusions The rat model of renal ischemia-reperfusion injury is established by clamping bilateral renal pedicles via dorsal retroperitoneal incision. This surgical procedure is stable and simple, with a high success rate and small incision, less bleeding, and minimal animal injury.