**3.6 VD3 modulates hippocampal NF-kB/p65/p65 and 17β-E2/VD3 receptors levels in long-term OVX rats treated with 17β-E2 exposed to CUMS**

CUMS significantly increased NF-kB/p65/p65 levels and decreased 17β-E2/VD3 receptors concentrations in the hippocampus of SHAM rats compared to the non-CUMS control (**Figure 7**, P < 0.05). CUMS produced a increase of hippocampal

#### **Figure 7.**

*VD3 modulates hippocampal NF-kB/p65 and 17β-E2/VD3 receptors levels in long-term OVX rats treated with 17β-E2 submitted to CUMS tested by ELISA. (a) NF-kB/p65/p65, μg/ml, (b) 17β-E2 receptor, pg/ml, and (c) VD3 receptor, pg/ml. \* – P < 0.05 versus the control group, # – P < 0.05 versus to the SHAM group with CUMS, \$ – P < 0.05 versus to the OVX group with CUMS, and \$\$ – P < 0.05 versus to the OVX group with CUMS treated with 17β-E2. The data are presented as mean ± SD; n = 7 in each group.*

**165**

**Figure 8.**

*Vitamin D3 Modulates NF-kB/p65, 17β-Estradiol, and Vitamin D Receptors Expression…*

NF-kB/p65/p65 and decrease of 17β-E2/VD3 receptors levels in the long-term OVX rats compared to the non-CUMS/CUMS SHAM rats (**Figure 7**, F(1,34) = 28.44, P < 0.05). Fluoxetine (10.0 mg/kg) decreased NF-kB/p65/p65 levels in the hippocampus of long-term OVX rats treated to CUMS compared to the OVX plus solvent/SHAM rats with CUMS (**Figure 7**, P < 0.05). Moreover, VD3 plus 17β-E2 reversed 17β-E2/VD3 receptors levels and reduced NF-kB/p65 levels in the hippocampus of the long-term OVX rats compared to OVX plus solvent or 17β-E2/SHAM rats with CUMS (**Figure 7**, P < 0.05). Fluoxetine failed to modify 17β-E2/VD3 receptors levels in the long-term

Western blotting analysis revealed that NF-kB/p65 protein levels in the hippocampus of SHAM rats submitted to CUMS were higher compared to non-CUMS control

*VD3 modulates hippocampal NF-kB/p65 and 17β-E2/VD3 receptors expressions in long-term OVX rats with 17β-E2 submitted to CUMS detected with western blotting treated. 1 – control SHAM, 2 – SHAM + CUMS + solvent, 3 – OVX + CUMS + solvent, 4 – OVX rats + CUMS + fluoxetine, 5 – OVX rats + CUMS + 17β-E2, and 6 – OVX rats + CUMS + VD3 + 17β-E2. \* – P < 0.05 versus the control group, # – P < 0.05 versus to the SHAM group with CUMS, \$ – P < 0.05 versus to the OVX group with CUMS, and \$\$ – P < 0.05 versus to the OVX group with CUMS treated with 17β-E2. The data are presented as mean ± SD; n = 7 in each group.*

*DOI: http://dx.doi.org/10.5772/intechopen.89357*

OVX rats exposed to CUMS (**Figure 7**, P > 0.05).

*Vitamin D3 Modulates NF-kB/p65, 17β-Estradiol, and Vitamin D Receptors Expression… DOI: http://dx.doi.org/10.5772/intechopen.89357*

NF-kB/p65/p65 and decrease of 17β-E2/VD3 receptors levels in the long-term OVX rats compared to the non-CUMS/CUMS SHAM rats (**Figure 7**, F(1,34) = 28.44, P < 0.05).

Fluoxetine (10.0 mg/kg) decreased NF-kB/p65/p65 levels in the hippocampus of long-term OVX rats treated to CUMS compared to the OVX plus solvent/SHAM rats with CUMS (**Figure 7**, P < 0.05). Moreover, VD3 plus 17β-E2 reversed 17β-E2/VD3 receptors levels and reduced NF-kB/p65 levels in the hippocampus of the long-term OVX rats compared to OVX plus solvent or 17β-E2/SHAM rats with CUMS (**Figure 7**, P < 0.05). Fluoxetine failed to modify 17β-E2/VD3 receptors levels in the long-term OVX rats exposed to CUMS (**Figure 7**, P > 0.05).

Western blotting analysis revealed that NF-kB/p65 protein levels in the hippocampus of SHAM rats submitted to CUMS were higher compared to non-CUMS control

#### **Figure 8.**

*Vitamin D Deficiency*

P > 0.05).

estradiol and VD3 levels in the long-term OVX rats exposed to CUMS (**Figure 6**,

CUMS significantly increased NF-kB/p65/p65 levels and decreased 17β-E2/VD3 receptors concentrations in the hippocampus of SHAM rats compared to the non-CUMS control (**Figure 7**, P < 0.05). CUMS produced a increase of hippocampal

*VD3 modulates hippocampal NF-kB/p65 and 17β-E2/VD3 receptors levels in long-term OVX rats treated with 17β-E2 submitted to CUMS tested by ELISA. (a) NF-kB/p65/p65, μg/ml, (b) 17β-E2 receptor, pg/ml, and (c) VD3 receptor, pg/ml. \* – P < 0.05 versus the control group, # – P < 0.05 versus to the SHAM group with CUMS, \$ – P < 0.05 versus to the OVX group with CUMS, and \$\$ – P < 0.05 versus to the OVX group with CUMS* 

*treated with 17β-E2. The data are presented as mean ± SD; n = 7 in each group.*

**3.6 VD3 modulates hippocampal NF-kB/p65/p65 and 17β-E2/VD3 receptors levels in long-term OVX rats treated with 17β-E2 exposed to CUMS**

**164**

**Figure 7.**

*VD3 modulates hippocampal NF-kB/p65 and 17β-E2/VD3 receptors expressions in long-term OVX rats with 17β-E2 submitted to CUMS detected with western blotting treated. 1 – control SHAM, 2 – SHAM + CUMS + solvent, 3 – OVX + CUMS + solvent, 4 – OVX rats + CUMS + fluoxetine, 5 – OVX rats + CUMS + 17β-E2, and 6 – OVX rats + CUMS + VD3 + 17β-E2. \* – P < 0.05 versus the control group, # – P < 0.05 versus to the SHAM group with CUMS, \$ – P < 0.05 versus to the OVX group with CUMS, and \$\$ – P < 0.05 versus to the OVX group with CUMS treated with 17β-E2. The data are presented as mean ± SD; n = 7 in each group.*

females (**Figure 8**, P < 0.05). NF-kB/p65 levels were increased in the hippocampus of long-term OVX rats with CUMS compared to the non-CUMS/CUMS SHAM rats (**Figure 8**, F(1,34) = 34.45, F(1,34) = 16.38, respectively, P < 0.05). Fluoxetine (10.0 mg/kg) resulted in significant reduced levels of hippocampal NF-kB/p65 protein expression in long-term OVX with CUMS compared to the OVX plus solvent/SHAM rats with CUMS (**Figure 8**, P < 0.05). Co-treatment with VD3 and 17β-E2 decreased NF-kB/p65 protein levels and increased 17β-E2/VD3 receptors protein expression in the hippocampus of the long-term OVX rats compared to OVX plus solvent or 17β-E2/ SHAM rats with CUMS (**Figure 8**, P < 0.05). Fluoxetine did not alter 17β-E2/VD3 protein expression in the long-term OVX rats exposed to CUMS (**Figure 8**, P > 0.05).
