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Sulforaphane Ameliorates Bladder Dysfunction through Activation of the Nrf2-ARE Pathway in a Rat Model of Partial Bladder Outlet Obstruction.

Liu C, Xu H, Fu S, Chen Y, Chen Q, Cai Z, Zhou J, Wang Z - Oxid Med Cell Longev (2016)

Bottom Line: SFN treatment also increased the activity of SOD, GSH-Px, and CAT compared to the other groups.Moreover, SFN could reduce the ratio of Bax/Bcl-2 expression.Conclusions.

View Article: PubMed Central - PubMed

Affiliation: Department of Urology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, China.

ABSTRACT
Purpose. We evaluated the effect of sulforaphane (SFN) treatment on the function and changes of expression of Nrf2-ARE pathway in the bladder of rats with bladder outlet obstruction (BOO). Materials and Methods. A total of 18 male Sprague-Dawley rats at age of 8 weeks were divided into 3 groups (6 of each): the sham operated group, the BOO group, and the BOO+SFN group. We examined histological alterations and the changes of oxidative stress markers and the protein expression of the Nrf2-ARE pathway. Results. We found that SFN treatment could prolong micturition interval and increase bladder capacity and bladder compliance. However, the peak voiding pressure was lower than BOO group. SFN treatment can ameliorate the increase of collagen fibers induced by obstruction. SFN treatment also increased the activity of SOD, GSH-Px, and CAT compared to the other groups. The level of bladder cell apoptosis was decreased in BOO rats with SFN treatment. Moreover, SFN could reduce the ratio of Bax/Bcl-2 expression. Furthermore, SFN could activate the Nrf2 expression with elevation of its target antioxidant proteins. Conclusions. The sulforaphane-mediated decrease of oxidative stress and activation of the Nrf2-ARE pathway may ameliorate bladder dysfunction caused by bladder outlet obstruction.

No MeSH data available.


Related in: MedlinePlus

Effect of SFN on the Nrf2-ARE pathway in BOO rats. (a) Immunohistochemical staining of Nrf2 and HO-1 in the bladder of the three groups. Original magnification ×200. (b) The protein expression of total Nrf2 in the bladder of the three groups. (c) The protein expression of nuclear Nrf2 in the bladder of the three groups. (d) The protein expression of HO-1 in the bladder of the three groups. (e) The protein expression of NQO1 in the bladder of the three groups. ∗P < 0.05 versus sham group. #P < 0.05 versus BOO group.
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fig5: Effect of SFN on the Nrf2-ARE pathway in BOO rats. (a) Immunohistochemical staining of Nrf2 and HO-1 in the bladder of the three groups. Original magnification ×200. (b) The protein expression of total Nrf2 in the bladder of the three groups. (c) The protein expression of nuclear Nrf2 in the bladder of the three groups. (d) The protein expression of HO-1 in the bladder of the three groups. (e) The protein expression of NQO1 in the bladder of the three groups. ∗P < 0.05 versus sham group. #P < 0.05 versus BOO group.

Mentions: The transcription factor Nrf2 is a vital mediator involved in regulating cellular antioxidative responses. As SFN might be an activator of Nrf2, we investigated the effects of SFN on the expression of Nrf2 and its downstream target proteins. As shown in Figure 5(a), immunohistochemical results demonstrated that the expression level of Nrf2 was significantly higher in the muscular layers of the bladder in the BOO+SFN group compared to the BOO group. More importantly, the expression of Nrf2 was mainly located in the nucleus of the bladder cells. The expression of Nrf2 in the cell and nucleus was also measured by western blotting (Figures 5(b) and 5(c)). The results showed that the expression of Nrf2 was significantly increased in the bladder of BOO+SFN group compared with the BOO group and the total Nrf2 was increased in the bladder of the BOO group compared to the sham group. However, the expression of Nrf2 in the nucleus showed no significant difference between the BOO group and the sham group, and the level of Nrf2 in the nucleus was markedly increased in the BOO+SFN group compared to the BOO group.


Sulforaphane Ameliorates Bladder Dysfunction through Activation of the Nrf2-ARE Pathway in a Rat Model of Partial Bladder Outlet Obstruction.

Liu C, Xu H, Fu S, Chen Y, Chen Q, Cai Z, Zhou J, Wang Z - Oxid Med Cell Longev (2016)

Effect of SFN on the Nrf2-ARE pathway in BOO rats. (a) Immunohistochemical staining of Nrf2 and HO-1 in the bladder of the three groups. Original magnification ×200. (b) The protein expression of total Nrf2 in the bladder of the three groups. (c) The protein expression of nuclear Nrf2 in the bladder of the three groups. (d) The protein expression of HO-1 in the bladder of the three groups. (e) The protein expression of NQO1 in the bladder of the three groups. ∗P < 0.05 versus sham group. #P < 0.05 versus BOO group.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4940551&req=5

fig5: Effect of SFN on the Nrf2-ARE pathway in BOO rats. (a) Immunohistochemical staining of Nrf2 and HO-1 in the bladder of the three groups. Original magnification ×200. (b) The protein expression of total Nrf2 in the bladder of the three groups. (c) The protein expression of nuclear Nrf2 in the bladder of the three groups. (d) The protein expression of HO-1 in the bladder of the three groups. (e) The protein expression of NQO1 in the bladder of the three groups. ∗P < 0.05 versus sham group. #P < 0.05 versus BOO group.
Mentions: The transcription factor Nrf2 is a vital mediator involved in regulating cellular antioxidative responses. As SFN might be an activator of Nrf2, we investigated the effects of SFN on the expression of Nrf2 and its downstream target proteins. As shown in Figure 5(a), immunohistochemical results demonstrated that the expression level of Nrf2 was significantly higher in the muscular layers of the bladder in the BOO+SFN group compared to the BOO group. More importantly, the expression of Nrf2 was mainly located in the nucleus of the bladder cells. The expression of Nrf2 in the cell and nucleus was also measured by western blotting (Figures 5(b) and 5(c)). The results showed that the expression of Nrf2 was significantly increased in the bladder of BOO+SFN group compared with the BOO group and the total Nrf2 was increased in the bladder of the BOO group compared to the sham group. However, the expression of Nrf2 in the nucleus showed no significant difference between the BOO group and the sham group, and the level of Nrf2 in the nucleus was markedly increased in the BOO+SFN group compared to the BOO group.

Bottom Line: SFN treatment also increased the activity of SOD, GSH-Px, and CAT compared to the other groups.Moreover, SFN could reduce the ratio of Bax/Bcl-2 expression.Conclusions.

View Article: PubMed Central - PubMed

Affiliation: Department of Urology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, China.

ABSTRACT
Purpose. We evaluated the effect of sulforaphane (SFN) treatment on the function and changes of expression of Nrf2-ARE pathway in the bladder of rats with bladder outlet obstruction (BOO). Materials and Methods. A total of 18 male Sprague-Dawley rats at age of 8 weeks were divided into 3 groups (6 of each): the sham operated group, the BOO group, and the BOO+SFN group. We examined histological alterations and the changes of oxidative stress markers and the protein expression of the Nrf2-ARE pathway. Results. We found that SFN treatment could prolong micturition interval and increase bladder capacity and bladder compliance. However, the peak voiding pressure was lower than BOO group. SFN treatment can ameliorate the increase of collagen fibers induced by obstruction. SFN treatment also increased the activity of SOD, GSH-Px, and CAT compared to the other groups. The level of bladder cell apoptosis was decreased in BOO rats with SFN treatment. Moreover, SFN could reduce the ratio of Bax/Bcl-2 expression. Furthermore, SFN could activate the Nrf2 expression with elevation of its target antioxidant proteins. Conclusions. The sulforaphane-mediated decrease of oxidative stress and activation of the Nrf2-ARE pathway may ameliorate bladder dysfunction caused by bladder outlet obstruction.

No MeSH data available.


Related in: MedlinePlus