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. 2021 May 21;12(6):523. doi: 10.1038/s41419-021-03813-6

Fig. 6. CD36 knockdown prevents tubulointerstitial inflammation in diabetic mice.

Fig. 6

A Representative photomicrographs of PAS staining, immunohistochemistry and TUNEL staining images in the db/m, db/db, db/db + NC, and db/db + kCD36 groups at 16 weeks (magnification: ×400). B Semiquantitative analyses of the proximal tubular area according to the outer diameter at 16 weeks. C Semiquantitative analyses of the tubulointerstitial damage index at 16 weeks. D Bar graph of the mean number of TUNEL-positive cells per group. E Semiquantitative analysis of MCP-1 and F4/80 from the immunohistochemical staining data (8–10 sections per mouse were analyzed) at 16 weeks. F Representative Western blot of CD36 and MCP-1 expression in the kidney. G The level of CD36 mRNA in the kidney tissue by RT-PCR. H Representative western blot of Bax, Bcl-2, and cleaved-caspase-3 expression in the kidney. db/m: normal male mice; db/db: diabetic mice; db/db + NC: db/db + NC lentivirus vectors (LV3-NC); db/db + kCD36: db/db + CD36 mutant lentivirus vectors (LV3-shRNA). Data are expressed as the means ± SD. (n = 6). **P < 0.01 versus the db/m group; #P < 0.05, compared with the db/db group by ANOVA.