Fig. 7: CD36 knockdown inhibits diabetes-induced oxidative stress, NLRP3 inflammasome formation, phosphorylation of AMPK, ACC, and expression of CPT1 in db/db mice. | Cell Death & Disease

Fig. 7: CD36 knockdown inhibits diabetes-induced oxidative stress, NLRP3 inflammasome formation, phosphorylation of AMPK, ACC, and expression of CPT1 in db/db mice.

From: CD36 promotes NLRP3 inflammasome activation via the mtROS pathway in renal tubular epithelial cells of diabetic kidneys

Fig. 7

A The level of urinary MDA was detected by ELISA. B The level of urinary 8-OHdG was detected by ELISA. C Level of mtROS expression in experimental animals was determined by FACS using MitoNeoD reagent. D Representative western blot and quantitative analysis of the level of CD36, NLRP3, caspase-1, and IL-1β expression in the kidney. E The level of p-AMPK, AMPK, p-ACC, ACC, and CPT1 protein expression was analyzed by western blot. 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. F Molecular mechanism by which CD36 stimulates activation of the NLRP3 inflammasome in renal TECs in DN. CD36 expression was enhanced, which occurred in the presence of high glucose. Inhibition of FAO through inactivation of the AMPK signaling pathway promotes decreased OXPHOS. Under HG conditions, the CD36-induced decrease in FAO facilitates increased glycolysis, an imbalance between FA uptake and consumption (FAO), and contributes to mtROS production, which activates the NLRP3 inflammasome signaling pathway.

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