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. Author manuscript; available in PMC: 2014 Jul 1.
Published in final edited form as: Andrology. 2013 May 20;1(4):651–659. doi: 10.1111/j.2047-2927.2013.00091.x

FIG. 2. HN stimulated STAT3 phosphorylation and decreased p38 MAP kinase activation in rat testis.

FIG. 2

FIG. 2

FIG. 2

Western blots for STAT3 phosphorylation and p38 MAPK activation in the rat testis total homogenates. A and B: GnRH-A treatment suppressed phosphorylation of STAT3 at both Tyr705 (A, top lane) and Ser727 (B, top lane). HN treatment restored both forms of phosphorylated STAT3. GAPDH was used as loading control (A, bottom lane and B, bottom lane), but STAT3 was used as normalization factor in density analysis (A, middle lane and B, middle lane). C: GnRH-A treatment induced activation of p38 MAPK which is reflected by phosphorylation of ATF2 in this assay. HN combined with GnRH-A treatment suppressed the increased p38 MAPK activation. ATF2 was used as sample control (normalization factor in density analysis). Values are means ± SD. Means with unlike superscripts are significantly (P<0.05) different.