Objective To investigate the effect of salidroside on brain edema and neurological function in global cerebral ischemia-reperfusion injury in rats.Methods A total of 100 Sprague Dawley rats were randomly divided into sham operation,ischemia-reperfusion and salidroside 12,24 and 48 mg/kg groups (n =20 in each group),and than redivided into 6 h,24 h,72 h and 7 dsubgroups (n =5 in each subgroup).A rat model of global cerebral ischemia was established using the four-vessel occlusion method.Immediately after modeling,all groups were administered intragastrically for 7 days.The brain water content was quantitated by the wet-dry weight method.The neurological evaluation was performed using a neurological deficit score (NDS).Results After modeling both the ischemia-reperfusion group and all the salidroside groups had significant neurological deficit,and as time went by,it was improved gradually.Compared to the ischemia-reperfusion group at the corresponding time points,neurological deficit in all the salidroside groups was improved significantly (all P ＜ 0.05),and showing a dose-dependent trend.Compared to the salidroside 12 mg/kg and 24 mg/kg groups,neurological deficit in the salidroside 48 mg/kg group was improved significantly at 72 hours and 7 days (all P ＜ 0.05).The brain water contents began to increase at 6 hours after modeling in the the ischemia-reperfusion group and all the salidroside group.They reached the peak at 72 hours,and significantly higher than that in the sham operation group (all P ＜ 0.05).The brain water contents in all the salidroside group were significantly lower than those in the ischemiareperfusion group at 24 and 72 hours after modeling (all P ＜ 0.05) and showing a dosedependent trend.The brain water content in the salidroside 48 mg/kg group was close to that in the sham operation group at 7 days after modeling.Conclusions Salidroside may significantlydecrease brain edema and improve neurological function in global cerebral ischemia-reperfusion injury in rats,and it has a neuroprotective effect.

OBJECTIVEInflammatory factors have been known to induce nerve cells apoptosis and decrease learning capacity of diabetics. The aim of this study is to evaluate the inhibitory effect of Gastrodine on the expression of interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6) in culturing for gitter cells (BV-2 cells) induced by high concentration of glucose.

METHODThe BV-2 cells incubated in vitro with different concentrations of glucose and gastrodine were divided into five groups: control group (glucose: 25 mmol x L(-1)), high concetration of glucose (glucose: 45 mmol x L(-1) HCG) group and Gastrodine groups (glucose 45 mmol x L(-1) with gastrodine 25 mg x L(-1) (LG), 50 mg x L(-1) (MG), 100 mg x L(-1) (HG). After culturing for 24 h, morphological changes of cells were observed by inverted phase contrast microscope. The supernatant protein of IL-1 beta and IL-6 was detected by ELISA. The mRNA expression of IL-1 beta and IL-6 was assessed by Reverse transcription polymerase chain reaction (RT-PCR).

RESULTThe cells were proned to aggregate, some of them with hypertrophy, distinct nucleoli and branch-shaped hyperplasy in HCG group, while less change in Gastrodine groups. The supernatant protein of IL-1 beta is higher in HCG group than control group (119.53 +/- 15.91) ng x L(-1) vs (25.74 +/- 15.72) ng x L(-1) (P < 0.01), but lower in the gastrodine groups than HCG LG (99.32 +/- 19.66) ng x L(-1), MG (76.94 +/- 17.16) ng x L(-1), HG (88.35 +/- 18.72) ng x L(-1) vs (119.53 +/-15.91) ng x L(-1) (P < 0.05). The supernatant protein of IL-6 protein also higher in HCG than control group (393.7 +/- 17.51) ng x L(-1) vs (125.85 +/- 36.62) ng x L(-1) (P < 0.01), and lower in the gastrodine groups than HCG (LG 327.06 +/- 23.53) ng x L(-1), MG (217.36 +/- 28.81) ng x L(-1), HG (263.17 +/- 22.32) ng x L(-1) vs (393.7 +/- 17.51) ng x L(-1), P < 0.05). The mRNA expression of IL-1 beta was increased significantly higher in HCG than control group (2.77 +/- 0.29) vs (1.13 +/- 0.27) (P < 0.05), but decreased significantly in gastrodine groups than HCG LGA (2.66 +/- 0.31), MGA (2.1 +/- 0.41), HGA (2.4 +/- 0.28) vs (2.77 +/- 0.29) (P < 0.05). The mRNA Expression of IL-6 was higher in HCG than control group (3.97 +/- 0.33) vs (1.05 +/- 0.13) (P < 0.05, but lower in gastrodine groups than HCG LG (3.28 +/- 0.3), MG (2.65 +/- 0.33), HG (3.04 +/- 0.26), vs (3.97 +/- 0.33) (P < 0.05).

CONCLUSIONGastrodine can inhibit the expression of IL-1 beta, IL-6 in cultured BV-2 cells induced by high concentration of glucose.

Animals ; Benzyl Alcohols ; pharmacology ; Cells, Cultured ; Down-Regulation ; Gene Expression ; drug effects ; Glucose ; metabolism ; Glucosides ; pharmacology ; Interleukin-1beta ; genetics ; metabolism ; Interleukin-6 ; genetics ; metabolism ; Mice ; Microglia ; drug effects ; metabolism