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. 2023 Apr 3;13(4):937. doi: 10.3390/life13040937

Figure 3.

Figure 3

Schematic representation of hesperidin bleomycin-induced experimental pulmonary fibrosis. (I) Hesperidin’s impact on modifications in rat lung Nrf2, HO-1, TNF-β, IL-1, and IL-6 mRNA expression brought on by BLM. (A) on day 14, quantitative representation of mRNA expression of Nrf2 (B), HO-1 (C), TNF-α (D), IL-1β (E) and IL-6 (F). p < 0.05 when compared with: sham group (&), normal group (#), each other (MP or hesperidin) group ($), and BLM control group (*). (II) Effect of hesperidin on BLM-induced modifications in the rats’ lungs’ and airways’ histology. This is magnified 400×. Photomicrograph of sections of lungs of normal (A), sham control (B), BLM control (C), MP (10 mg/kg) treated (D), hesperidin (50 mg/kg) treated (E), hesperidin (100 mg/kg) treated (F) and Perse treated (G) rats. Lung H&E staining (1A–1G) on day 14, Lung Picro-Sirius red staining (2A–2G) on day 28 and Lung Masson’s trichrome staining (3A–3G) on day 28. Effect of hesperidin on alterations induced by BLM in lung airway inflammation score (H), Ashcroft Score (I) and interstitial fibrosis score (J). p < 0.05 when compared with: sham group (&), normal group (#), each other (MP or hesperidin) group ($), and BLM control group (*). (n = 3) (III) BLM altered rats’ lung ultrastructure, which was inhibited by hesperidin. Photomicrographs of lung from representative animals, normal (at 3474×) (A), sham control (at 11,580×) (B), BLM control (at 7720×) (C), methylprednisolone (10 mg/kg) treated (at (11,580×) (D), hesperidin (100 mg/kg) treated (at 13,510×) (E), and per Se treated rats (at 11,500×) (F) [34].