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. 2018 Jun 7;16(2):867–873. doi: 10.3892/etm.2018.6258

Figure 4.

Figure 4.

NGN inhibited ACE1 protein expression in myocardial tissue in rats with L-NAME-induced hypertension. (A) Analysis of angiotensinogen, ACE1, ACE2 and AT1R mRNA expression by reverse transcription-quantitative polymerase chain reaction in myocardial tissue from rats treated with vehicle (control), L-NAME, or L-NAME + NGN for 8 weeks. (B) Representative western blots of ACE1, AT1R and AT2R in myocardial tissue from rats in the control, L-NAME, and L-NAME + NGN groups 8 weeks after L-NAME administration. (C) Analysis of ACE1, AT1R and AT2R protein expression by western blot analysis. (D) Immunohistochemistry was used to detect ACE1 in serial paraffin sections of myocardial tissue from rats with L-NAME-induced hypertension. The insets show high-magnification images of the rectangular areas in each panel. The black arrowheads indicate strong ACE1 expression. (E) Analysis of ACE1 protein expression by immunohistochemistry n=10. The data are expressed as mean ± standard error of the mean. **P<0.01, ***P<0.001. NGN, naringenin; ACE, angiotensin-converting enzyme; AGT, angiotensinogen; AT1R, angiotensin II receptor type 1; AT2R, angiotensin II receptor type 2; L-NAME, NG-nitro-L-arginine methyl ester.