Aim To investigate the neuroprotective effect of salidroside in MCAO rats. Methods The rats were subjected to middle cerebral artery occlusion with suture-occluded method, and the neurologic injury and infarct size of rats were evaluated. According to the gene chip detected, the protein expressions of caspase-3 , cleaved caspase-3 were determined and the mRNA expressions of IL-6, Vgf, Hba-a2, Hbb-b1, Hbb, CD44, Pnpla2, Slc6a5 and Slc5a7 were tested. Re-sults Compared with MCAO group, salidroside signif-icantly improved the neurological deficit, reduced the infarct sizes, inhibited the expressions of cleaved caspase-3 protein and IL-6 mRNA, promoted the ex-pressions of Vgf, Hba-a2, Hbb-b1, Hbb, and reduced the expressions of CD44 , Pnpla2 , Slc6 a5 and Slc5 a7 . Conclusions Salidroside can reduce the neurological deficit and infarct size, and protect rats against focal cerebral ischemia-reperfusion injury, which may be ac-complished by increasing the expressions of Vgf, Hba-a2, Hbb-b1, and Hbb, and decreasing the expressions of cleaved caspase-3 , IL-6 , CD44 , Pnpla2 , Slc6 a5 and Slc5 a7 .

Aim To investigate the effect of Salidroside on the focal celebral ischemia/reperfusion injury in rats and its underlying mechanism. Methods Adult male Sprague-Dawley rats, weighing 260-300 g, were ran-domly divided into three groups: sham, MCAO, MCAO+salidroside ( Sal ) groups. The rats were sub-jected to local celebral ischemia reperfusion with su-
ture-occluded method. The rats of MCAO +Sal group were treated intraperitoneally with salidroside ( 50 mg ·kg-1 ) for 6 days. Neurological deficit testing was performed with Longa’ s Scale. The mRNA expressions of Neun,Nogo-A,and NgR were detected by RT-qPCR in ischemic brain. The protein expressions of Neun, NGF , BDNF , Nogo-A and NgR were determined by
Western blot. Results Compared with MCAO group, salidroside significantly improved the neurological defi-cit,promoted the expressions of Bcl-2,Neun,NGF,BD-NF, and inhibited the expressions of Nogo-A, NgR. Conclusion Salidroside can reduce neurological defi-cit, increase the number of Nissl’ s Body and the ex-pression of Neun, and protect rats against focal cele-
bral ischemia/reperfusion injury,which may be accom-plished by increasing the expressions of Bcl-2, NGF, BDNF, and inhibiting the expressions of Nogo-A, NgR.

Aim To investigate glucose uptake effects and mechanism of emodin in 3T3-L1 adipocytes. Methods LPS-induced differentiated 3 T3-L1 adipo-cytes were divided into control group and emodin ( 1 , 10, 50 μmol · L-1 ) groups. Then, 6-NBDG uptake and the expression of cell surface GLUT4 , PPARγ, AMPKα1/2 , p-AMPKα1/2 , IRS-1 , p-IRS-1 , Adi-ponectin, chREBP-α and chREBP-β were detected. The ability of 6-NBDG uptake in LPS-induced 3 T3-L1 adipocytes was also evaluated following interference with AMPK inhibitor and PPARγinhibitor, respective-ly. Meanwhile, STZ-induced diabetic rats were ran-domly divided into control group and emodin treatment group. The mRNA expression of Adiponectin and pro-tein expression of cell surface GLUT4 , AMPKα1/2 , p-AMPKα1/2 were measured. Results Compared with the control group, emodin improved the mRNA expres-sion of cell surface GLUT4, Adiponectin, chREBP-αand chREBP-β, and protein expression of cell surface GLUT4 , PPARγ, IRS-1 , p-IRS-1 , AMPKα1/2 and p-AMPKα1/2 in 3T3-L1 adipocytes(P<0. 05). Emodin enhanced 6-NBDG uptake and the uptake of emodin group was both decreased following interference with AMPK inhibitor and PPARγ inhibitor, respectively ( P<0. 05 ) . Emodin also increased the mRNA expression of Adiponectin and protein expression of cell surface GLUT4 , AMPKα1/2 and p-AMPKα1/2 in adipose tis-sue of T2 DM rats ( P <0. 05 ) . Conclusion Emodin can enhance glucose uptake in 3 T3-L1 adipocytes and the mechanism is probably associated with activating Adiponectin and IRS-1 , thereby activating AMPK and PPARγ.