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. 2020 Aug;8(16):990. doi: 10.21037/atm-20-5548

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2020 Annals of Translational Medicine. All rights reserved.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0.

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Tet relieves pathological histological and tissue apoptosis in the kidneys via regulating the expression of Ki67 and survivin. Pathological damage was detected by HE, and apoptosis was detected by TUNEL. (A) Representative pictures of HE (×200) and TUNEL (×200). (B) Percentage of apoptosis cells. Relative expression of Ki67 and survivin on protein levels were detected by Western blot. (C) Representative pictures of Western blot. (D,E) The relative protein level of Ki67 and survivin. (**, P<0.01 versus the control group; ^#, P<0.05; ^##, P<0.01 versus the DN model group). DN, diabetic nephropathy; Tet, tetrandrine; TUNEL, terminal-deoxynucleoitidyl transferase mediated nick end labeling.