The effects of dexmedetomidine on the cognitive function and TGF β/Smad pathway in propofol-anesthetized rats

Objective: To investigate the effects of dexmedetomidine on the cognitive function and the TGF-β/Smad pathway in propofol-anesthetized rats. Methods: A total of 36 20-month-old Sprague-Dawley (SD) rats were randomly assigned to the following three groups: the dexmedetomidine + propofol anesthetized group (D group), the propofol-anesthetized group (P group), or the blank control group (C group). The rats in D group were infused with dexmedetomidine and propofol via the caudal vein using an infusion pump for 4 hours, those in P group received an infusion of propofol alone via the caudal vein for 4 hours, but those in C group did not receive any treatment. All the rats in D and P groups underwent exploratory laparotomies. Morris water maze experiments were conducted on the rats on the 1st, 3rd, and 5th days after surgery. The rats were sacrificed on the 6th day, and then some serum and hippocampal tissues were collected. The protein expressions (TGF-β1, Smad3, and Smad7) associated with the TGF-β/Smad pathway were measured using an enzyme linked immunosorbent assay (ELISA). Results: During the water maze experiment, compared with C group, the escape latencies of the rats in D and P groups were significantly prolonged, the time spent in finding the target quadrant was significantly shortened, and the number of times crossing the platform were considerably reduced (all P<0.05). D group showed significantly shorter escape latency, a remarkably longer time spent in finding the target quadrant, and significantly more times crossing the platform than the P group (P<0.05). Compared with C group, D and P groups had significantly elevated levels of TGF-β1, Smad3, and Smad7 in their serum and hippocampal tissues (all P<0.05); however, the levels of the above-mentioned proteins were markedly lower in D group than in P group (P<0.05). Conclusion: Anesthesia with propofol alone led to postoperative cognitive dysfunction (POCD) in elderly rats; however, the addition of dexmedetomidine relieved POCD and elevated the levels of proteins associated with the TGF-β/Smad pathway in the serum and hippocampal tissues of the propofol-anesthetized rats, suggesting that the TGF-β/Smad pathway was activated, and the addition of dexmedetomidine to propofol anesthesia reduced the protein levels. Hence, we speculate that dexmedetomidine relieves POCD in elderly rats by inhibiting the TGF-β/Smad pathway.