Effect of isoflurane and sevoflurane on hippocampal expressions of p-JNK, p-P38 and p-tau in aged rats after intracerebroventricular injection of amyloid-beta protein

Objective To investigate the effect of Isoflurane and Sevoflurane on hippocampal expressions of pJNK, p-P38 and p-tau in aged rats after intracerebroventricular injection of amyloid-beta protein. Methods Eighty rats at 20 months of life were randomly divided into 8 groups. Intracerebroventricular injection of 10 μl normal saline (control group), or Aβ1-40 monomer (Aβ1 group), or soluble Aβ1-40 oligomer (Aβ2 group) or insoluble Aβ1-40 fiber (Aβ3 group) was given. Rats in groups I+NS and I+Aβ1 inhaled 1.3 MAC isoflurane for 4 h after the injection of NS or Aβ1-40 monomer, while those in groups S+NS and S+Aβ1 inhaled 1.3 MAC sevoflurane for 4 h after the injection of NS or Aβ1-40 monomer, respectively. The animals were killed after two weeks and the hippocampus was harvested to determine the expressions of p-JNK, p-P38 and p-tau using Western-blot techniques. Results The expressions of p-JNK and p-P38 was significantly higher in groups Aβ2,Aβ3, I+NS, I+Aβ1 and S+Aβ1 while p-P38 was significantly higher only in S+NS (P0.05). The expression of p-tau was positive in groups Aβ2, Aβ3, I+Aβ1 and S+Aβ1 but not in others. Conclusion Both isoflurane and sevoflurane may enhance production of neurotoxic substance resulting from oligomerization of soluble Aβ1-40 in brain tissue, which can lead to even more harmful effects on signaling pathway.