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. 2021 May 7;24(6):102521. doi: 10.1016/j.isci.2021.102521

Figure 2.

Figure 2

Protective effects of CAN in the hearts of HFD/STZ-induced diabetic mice

(A) Morphology of the hearts from the HFD/STZ-induced diabetic mice was measured using pathological slices.

(B and C) (B) WGA and (C) Masson staining using pathological slices in the hearts of the HFD/STZ-induced diabetic mice.

(D–F) (D) Representative M-mode echocardiographic images; (E) left ventricular internal diastolic diameter (LVIDd), (F) left ventricular internal systolic diameter (LVIDs), and (G) ejection fraction detected by echocardiography (n = 4–5).

(H–M) (H) BNP, (I) CK, and (J) LDH levels in the serum detected by biochemical kits (n = 10). mRNA expression levels of the inflammatory factors, (K) Il-1α, (L) Il-6, and (M) Tnf-α in the hearts of the HFD/STZ-induced diabetic mice were determined using reverse transcription-quantitative PCR (n = 3). Data are presented as the mean ± SD. #p < 0.05 and ##p < 0.01 versus normal; ∗p < 0.05 and ∗∗p < 0.01 versus HFD/STZ. H&E, hematoxylin and eosin; BNP, B-type natriuretic peptide; CK, creatine kinase; LDH, lactate dehydrogenase; HFD, high-fat diet; STZ, streptozotocin; CAN, canagliflozin; normal, normal control group. HFD/STZ, HFD/STZ-induced diabetic control group; HFD/STZ + CAN, canagliflozin-treated HFD/STZ-induced diabetic group.