OBJECTIVE： To study the improvement effect of Shenrong bunao capsule on learning and memory ability of Alzheimer’s disease （AD） model mice， and to investigate its mechanism. METHODS： Totally 72 mice were randomly divided into blank control group （normal saline）， model group （normal saline）， Piracetam tablets group （positive control，0.80 g/kg），Shenrong bunao capsule high-dose，middle-dose and low-dose groups （1.92， 0.96， 0.48 g/kg）， with 12 mice in each group. Except that blank control group was given constant volume of normal saline subcutaneously. Other groups were given D-galactose （150 mg/kg） subcutaneously and sodium nitrite （50 mg/kg） intraperitoneally every day to induce AD model. At the same time，they were given relevant medicine intragastrically，once a day， for consecutive 60 d. 1 h after last administration， Morris water maze test was used to measure escape latency and times of crossing the platform within 90 s. HE staining was used to observe pathological changes of cerebral cortex in mice. Immunohistochemistry was used to detect the expressions of TNF-α， NF-κB p65， PI3K and Akt in cerebral cortex of mice. RESULTS： Compared with blank control group， escape latency was prolonged significantly （P＜0.01）， and the times of crossing the platform within 90 s was decreased significantly in model group （P＜0.01）. The neurons in cerebral cortex was damaged obviously， and the number of intact neurons was decreased significantly （P＜0.01）. The protein expressions of TNF-α， NF-κB p65， PI3K and Akt in cerebral cortex were increased significantly （P＜0.01）. Compared with model group， except that there was no statistical significance in escape latency， protein expressions of TNF-α， NF-кB p65， PI3K and Akt in Shenrong bunao capsule low-dose group （P＞0.05）， above indexes of other administration groups were improved significantly （P＜0.05 or P＜0.01）. CONCLUSIONS： Shenrong bunao capsule can improve the learning and memory ability of AD model mice， and its mechanism may be related to the inhibiting the protein expressions of TNF-α，NF-κB p65， PI3K and Akt in cerebral cortex region and relieving inflammation injury so as to protect cranial nerve.

OBJECTIVE To study the intervention effects and mechanism of Compound yu ’e nasal drops on ovalbumin induced allergic rhinitis in rats . METHODS The allergic rhinitis model of rat was induced with ovalbumin . Model rats were randomly divided into model group ，triamcinolone acetonide group （positive control ，0.026 mg/kg），Compound yu ’e nasal drops high-dose，medium-dose and low -dose groups （134.4、67.2、33.6 mg/kg），12 rats in each group . Another blank control group was set. Except for blank control group ，the corresponding drugs were given by nasal drip twice a day for 14 days. One hour after last administration，the nasal symptom scores of rats were recorded ；the levels of serum immunoglobulin E （IgE），interleukin-2（IL- 2），IL-13 and tumor necrosis factor -α（TNF-α）were measured by enzyme -linked immunosorbent assay . The changes of nasal mucosa in rat were observed by HE staining . The expressions of TNF -α，IL-2 and IL -13 in nasal mucosa were detected by Western blot. RESULTS Compared with blank control group ，nasal symptom score and the levels of serum IgE ，IL-2，IL-13，TNF-α in model group were increased significantly （P＜0.01）；obvious pathological injury was found in nasal mucosa ，and the expressions of TNF -α，IL-2 and IL -13 protein were increased significantly （P＜0.01）. Compared with model group ，Compound yu ’e nasal drops significantly reduced the nasal symptom score ，the levels of serum IgE ，IL-2，IL-13，TNF-α to different extents ，improved pathological injury of nasal mucosa and significantly inhibited the expressions of TNF -α，IL-2 and IL -13 protein（P＜0.05 or P＜ 0.01）. CONCLUSIONS Compound yu ’e nasal drops play significant effects against allergic rhinitis in rats by regulating the balance of t ype 1 helper T cells/type 2 helper T cells ，balancing and inhibiting the secretion of inflammatory cytokines .