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Sari et al. | Journal of Clinical and Translational Research 2024; 10(4): 246-255   251

                                    A                        B









                         C                       D                       E










        Figure 5. Haematoxylin and eosin staining of the cross-sectional tissue slices of the rat’s left ventricle: (A) normal rat tissue; (B) HF/HG/STZ;
        (C) HF/HG/STZ+EMPA; (D) HF/HG/STZ+VitD; and (E) HF/HG/STZ+EMPA+VitD. Scale bars: 50 µm. Magnification: ×400
        Abbreviations: HF/HG/STZ: High-fat/high-glucose/streptozotocin; EMPA: Empagliflozin; VitD: Vitamin D















        Figure 6. Additive effect of combination therapy on reducing   Figure 8. Synergistic effect of combination therapy on reducing
        cardiomyocyte cross-sectional area                     TGF-β mRNA expression
        Abbreviations: HF/HG/STZ: High-fat/high-glucose/streptozotocin;   Abbreviations: HF/HG/STZ: High-fat/high-glucose/streptozotocin;
        EMPA: Empagliflozin; VitD: Vitamin D                   EMPA: Empagliflozin; VitD: Vitamin D; TGF-β: Transforming
                                                               growth factor-β


















        Figure 7. Effect of EMPA, VitD, and combination therapy on TGF-β
        mRNA expression
        Abbreviation: HF/HG/STZ: High-fat/high-glucose/streptozotocin;   Figure 9. Effect of EMPA, VitD, and combination therapy on collagen
        EMPA: Empagliflozin; VitD: Vitamin D; TGF-β: Transforming   deposition
        growth factor-β                                        Abbreviation: HF/HG/STZ: High-fat/high-glucose/streptozotocin;
                                                               EMPA: Empagliflozin; VitD: Vitamin D
        Type I and III collagen, is a characteristic of cardiac fibrosis in
        T2DM. Similarly, the expression of cardiac TGF-β is associated   in experimental T2DM, suggesting a prominent role of TGF-β
        with  collagen  deposition,  myocardial  stiffness,  and  diastolic   signaling in  the  pathogenesis  of  DM-related  heart  failure  [7].
        dysfunction in diabetic rats [6]. Previous findings demonstrated   Therefore, we measured the expression of TGF-β mRNA and
        that diastolic dysfunction was ameliorated by inhibition of TGF-β   collagen deposition to quantitatively assess cardiac fibrosis.

                                               DOI: http://doi.org/10.36922/jctr.24.00010
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