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. 2022 Apr 22;100(5):781–795. doi: 10.1007/s00109-022-02184-5

Fig. 2.

Fig. 2

Inhibition of p38 MAPK does not alter development of hyperglycemia but prevents hyperglycemia-induced albuminuria. a Blood glucose levels of normoglycemic (control), hyperglycemic (STZ), and hyperglycemic mice treated with p38 MAPK inhibitor (STZ + SB202190) at day 1 and day 5. Glucose levels day 5: control (n = 11) vs. STZ (n = 14): 161.0 ± 5.6 vs. 341.6 ± 25.3 mg/dL (****p < 0.0001); STZ (n = 14) vs. STZ + SB202190 (n = 16): 341.6 ± 25.3 vs. 302.1 ± 18.8 mg/dl (p = ns). b Molecular mass markers are indicated in kilodalton (kDa), SDS-PAGE/Coomassie gel staining of urine (day 5) in normoglycemic (control), hyperglycemic (STZ), and hyperglycemic mice treated with p38 MAPK inhibitor (STZ + SB202190). BSA at 1, 5, and 10 µg/µL served both as a control and standard. c Quantitative analysis of the urinary albumin to creatinine ratio (UACR) (day 5) in normoglycemic (control), hyperglycemic (STZ), and hyperglycemic mice treated with p38 MAPK inhibitor (STZ + SB202190). UACR day 5: control (n = 18) vs. STZ (n = 15) 15.6 ± 3.0 vs. 152.9 ± 14.3 mg/g (****p < 0.0001); STZ (n = 15) vs. STZ + SB202190 (n = 8): 152.9 ± 14.3 vs. 53.5 ± 4.7 mg/g (****p < 0.0001)