The effects of salidroside on cognitive function and expression of inflammatory factor in diabetic rats / 中国中西医结合急救杂志

ABSTRACT

Objective To observe the effect of salidroside on the cognitive dysfunction of rats with diabetes induced by streptozotocin (STZ) and to explore its related mechanisms. Methods According to the random number table method, 45 Sprague-Dawley (SD) rats were divided into three groups the normal control, diabetic model and salidroside groups, 15 rats in each group. The diabetic rat model was established by intra-peritoneal injection of 60 mg/kg STZ (72 hours after STZ injection, the caudal venous blood glucose was measured by a glucose meter, if the glucose level reached ＞16.7 mmol/L , the model was regarded as a successful one). The rats in the normal control group were injected with equal volume of citrate buffer. After model making, the salidroside group was treated with salidrosidec 15 mg/kg by intragastric administration; the normal control group and the diabetic model group were given the same volume of normal saline for gavage, 1 times a day. Morris water maze was used to test cognitive function in rats after consecutive four weeks of treatment, and the blood glucose levels of rats in various groups were detected at the onset and the end of the experiment; the protein expression and contents of tumor necrosis factor-α (TNF-α) and intedeukin-6 (IL-6) in hippocampus were detected by enzyme linked immunosorbent assay (ELISA) and Western Blot analysis. Results Compared with the normal control group, the escape latency in diabetic model group was significantly prolonged (seconds 62.54±7.67 vs. 19.37±4.23), the time in target quadrant was shortened (seconds18.76±4.75 vs. 43.09±8.09), the number of crossing platform was also obviously reduced (frequency 2.26±0.57 vs. 6.84±1.56), blood glucose levels were significantly higher (mmol/L 24.27±3.69 vs. 6.95±1.52), protein expressions and contents of TNF-α and IL-6 in hippocampus were markedly increased [TNF-α (μg/L) 482.09±45.72 vs. 92.53±14.84, IL-6 (μg/L) 8.26±1.14 vs. 3.03±0.48; TNF-α protein (A value) 0.61±0.15 vs. 0.25±0.04, IL-6 protein (A value) 0.53±0.11 vs. 0.12±0.03, all P ＜ 0.05]. Compared with the diabetic model group, the escape latency in salidroside group was significantly shortened (seconds 38.07±5.84 vs. 62.54±7.67), the time in target quadrant was prolonged (seconds 31.29±5.61 vs. 18.76±4.75), the number of crossing platform was also significantly increased (frequency 4.72±1.24 vs. 2.26±0.57), blood glucose levels were obviously lowered (mmol/L 18.34±2.75 vs. 24.27±3.69), protein content and expression of TNF-α and IL-6 in hippocampus were remarkably decreased [TNF-α (μg/L) 328.46±39.33 vs. 482.09±45.72, IL-6 (μg/L) 6.09±0.97 vs. 8.26±1.14; TNF-α protein (A value)0.47±0.09 vs. 0.61±0.15, IL-6 protein (A value) 0.28±0.06 vs. 0.53±0.11, all P ＜ 0.05]. Conclusion Salidroside can ameliorate the cognitive impairment in STZ-induced diabetic rats, and its mechanism may be closely related to the reduction of the hippocampal inflammatory response and blood glucose level of diabetic rats.