Abstract: Objective  To explore the effect of microRNA-326 by targeting Kallikrein 7(Klk7) to regulate the mitogen activated protein kinase(MAPK) signaling pathway on depression model rats. 
Methods  A total of 20 SD rats were randomly divided into blank control group and chronic unpredictable mild stress(CUMS) group, with 10 rats in each group. CUMS was used to induce and prepare a rat model of depression. Sucrose preference test, open field test and forced swimming test were used to detect the behavioral changes of rats. Immunohistochemical was employed to detect Klk7 expression and TUNEL staining was used to detect apoptosis. Luciferase reporter gene experiment was used to verify the targeted binding between miR-326 and Klk7, and CCK-8 was used to detect the cell viability of hippocampal neurons. Real-time quantitative PCR and Western blot were used to detect the expression of miR-326 and Klk7, and Western blot was used to detect protein expression of Klk7 and MAPK signaling pathway related gene. 
Results  Compared with the blank control group, the sucrose preference value and the number of crossings of the CUMS group were significantly down-regulated(P＜0.05), while the resting time, Klk7 expression and apoptosis were significantly up-regulated(P＜0.05). Klk7 was a target gene of miR-326. Compared with the negative control(NC) group, miR-326 inhibited the activation of MAPK signaling pathway by targeting Klk7, thereby promoting the proliferation of hippocampal neurons in CUMS rats and inhibiting apoptosis(P＜0.05). Compared with miR-326 inhibitor group, miR-326 and Klk7 were simultaneously down-regulated to inhibit the activation of MAPK signaling pathway, promote the proliferation of hippocampal neurons in CUMS rats, and inhibit apoptosis(P＜0.05). 
Conclusion  MicroRNA-326 exerts a neuroprotective effect on depression model rats by targeting Klk7 to regulate MAPK signaling pathway.

Key words: depressive disorder, MAP kinase signaling system, rats