Abstract

Objective To explore the protective effects of Saikosaponin a (SSa) on cognitive function and mechanisms in rats after traumatic brain injury. Methods Sixty SD male rats were randomized into three groups: sham operation group (group S, n=20), trauma group (group T, n=20) and SSa treatment group (group A, n=20). SSa 5 mg/kg (group A) or equal volume saline (group S, group T) were administered by intraperitoneal injection in rats once daily for 5 consecutive days before trauma. Ten rats were selected randomly in each group for detecting hippocampal protein levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) by enzyme linked immunosorbent assay (ELISA). For the remaining rats in each group, the cognitive function was detected by Morris water maze test at 3, 4, 5 and 6 d after trauma. The hippocampal tissues were harvested after behavioral tests and homogenized for measuring the levels of brain derived neurophic factor (BDNF) by ELISA. Results The escape latency and swimming distance in group T at 3, 4, 5, 6 and 7 d after trauma were [ (81±6), (74±9), (66±5), (56±8), (44±5) s; (1 047±106), (886±78), (734±81), (620±58), (507±53) cm], those in group S significantly lower [ (65±8), (56±6), (41±5), (28±5), (14±5) s; (826±63), (674±52), (552±50), (389±36), (229±28) cm] than group T (P=0.008; P=0.011); The escape latency and swimming distance in group A at 3 and 4 d after trauma were [ (78±9), (67±8) s; (998±101), (826±83) cm], those in group S significantly lower [ (65±8), (56±6) s; (826±63), (674±52) cm] than group A (P=0.012; P=0.009); The escape latency and swimming distance in group A at 5, 6 and 7 d after trauma were [ (48±5), (32±5), (21±5) s; (628±59), (425±45), (294±31) cm], those in group T significantly prolonged [ (66±5), (56±8), (44±5) s; (734±81), (620±58), (507±53) cm] than group A (P=0.013; P=0.010). The levels of IL-6 and TNF-α in group T were [ (84±7), (150±9) pg/g], significantly higher than that of group S [ (44±4), (60±7) pg/g] (P=0.001; P=0.002) and group A [ (53±5), (76±7) pg/g] (P=0.001; P=0.001); The level of BDNF in group T was (366±42) pg/ml, significantly lower than that of group S (738±78) pg/ml (P=0.001) and group A (612±58) pg/ml (P=0.001). Conclusion SSa can significantly improve cognitive dysfunction in rats after traumatic brain injury, and the mechanism may be related to the inhibition of hippocampal inflammatory responses and activation of expression of cognitive function related protein. Key words: Saikosaponin A; Traumatic brain injury; Cognitive function; Inflammatory response

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call