Effects of salidroside on the cognitive function and expression of nuclear factor-κB, hypoxia-inducible factor-1α, apopto- sis-related proteins after operation

Objective To investigate the effects of salidroside (SAL) on the cognitive function and expression of nuclear factor-κB(NF-κB), hypoxia-inducible factor-1α (HIF-1α) and apoptosis-related proteins in the hippocampus of aged mice after partial hepatectomy, and to discusse the role of NF-κB, HIF-1α and apoptosis-related proteins [B-cell lymphoma-2 (Bcl-2), Bcl-2 related X protein (Bax) and caspase-3] in the pathogenesis of post-operative cognitive dysfunction (POCD). Methods Forty eight healthy male C57B/6 mice, aged 18 months, weight 25-35 g, were used in the study. These mice were randomly divided into three groups (n=16), using a random number table: a sham operation group (a sham group), an operation+normal saline group (an operation group) and a SAL group. Each group was subdivided into two groups (n=8) according to the test time points after operation: a 1 d after operation group and a 3 d after operation group. An operation model was established by partial hepatectomy in the operation and SAL groups. Mice in the SAL group were intraperitoneally injected with SAL. Mice in the sham group were incised and sutured at the same surgical site with partial hepatectomy. The Morris water maze was used to determine learning and memory ability. The hippocampi of these mice were isolated for detection of the expression of NF-κB, HIF-1α, Bcl-2, Bax and caspase-3 by Western blot. Results Compared with those in the sham group, the escape latency for mice in the operation group 1 and 3 days after operation obviously prolonged and the times to cross the platform decreased. Further-more, the expression of hippocampal NF-κB, HIF-1α, Bax and caspase-3 significantly increased, with a decreased level of Bcl-2 (P< 0.01). Compared with those in the operation group, the escape latency of the SAL group obviously decreased and the times to cross the platform increased. The expression of hippocampal NF-κB, HIF-1α, Bax and caspase-3 significantly decreased, with an increased level of Bcl-2 (P<0.05). Conclusions The pathogensis of POCD is associated with the expression of hippocampal NF-κB, HIF-1α and apoptosis-related proteins. SAL can improve the cognitive function of mice after partial hepatectomy through inhibiting the expression of NF-κB, HIF-1α and apoptosis-related proteins. Key words: Salidroside; Nuclear factor-κB; Hypoxia inducible factor-1α; Apoptosis, neurons; Post-operative cognitive dysfunction