Potential protective effect of hesperidin on hypoxia/reoxygenation‑induced hepatocyte injury

Abstract

Hesperidin (HDN) has been reported to have hydrogen radical-and hydrogen peroxide-removal activities and to serve an antioxidant role in biological systems. However, whether HDN protects hepatocytes (HCs) against hypoxia/reoxygenation (H/R)-induced injury remains unknown. The present study aimed to explore the role of HDN in H/R-induced injury. HCs were isolated and cultured under H/R conditions with or without HDN treatment. HC damage was markedly induced under H/R, as indicated by cell viability, supernatant lactate dehydrogenase levels and alanine aminotransferase levels; however, HDN treatment significantly reversed HC injury. Oxidative stress markers (malondialdehyde, superoxide dismutase, glutathioneand reactive oxygen species) were increased markedly during H/R in HCs; however, this effect was significantly attenuated after exposure to HDN. Compared with those of the control group, the mRNA expression levels of IL-6 and TNF-α in HCs and the concentrations of IL-6 and TNF-α in the supernatants increased significantly following H/R, and HDN significantly ameliorated these effects. Western blotting demonstrated that microtubule-associated protein 1 light chain 3α (MAP1LC3A, also known as LC3) and Beclin-1 protein expression levels increased, while sequestosome 1 levels decreased during H/R following exposure to HDN. The number of GFP-LC3 puncta in HCs following exposure to HDN was increased compared with that observed in HCs without HDN exposure under the H/R conditions after bafilomycin A1 treatment. In summary, the present study demonstrated that HDN attenuated HC oxidative stress and inflammatory responses while enhancing autophagy during H/R. HDN may have a potential protective effect on HCs during H/R-induced injury.

Systemic Dietary Hesperidin Modulation of Osteoclastogenesis, Bone Homeostasis and Periodontal Disease in Mice

“…For the higher dose of HE, the clear overexpression of p62 throughout culture, together with no clear increase in LC3-IIB conversion despite increase in LC3 towards end of differentiation, ERK 1/2 phosphorylation reduction (at day 5) and a decrease in number of apoptotic cells suggest that HE may present the ability to prolong the survival of those cells; however, they are not able to sustain autophagy which can impair full osteoclast differentiation and function [40]. Li et al (2021) [41], evaluating the potential in vitro protective effect of HE (50 µg/mL) on hypoxia/reoxygenation (H/R)induced hepatocyte injury, found that the protein levels of autophagy markers LC3-IIB and Beclin-1 increased, while p62 levels decreased during H/R under exposure to HE. The authors suggested that HE induces autophagy to protect the hepatocyte against H/R injury.…”

Hesperidin Exhibits Protective Effects against PM2.5-Mediated Mitochondrial Damage, Cell Cycle Arrest, and Cellular Senescence in Human HaCaT Keratinocytes

“…Hesperidin (3, 5, 7-trihydroxyflavone 7-rhamnoglucoside) is the main polyphenol compound found in citrus fruits. This bioflavonoid exhibits antioxidant, anti-inflammatory, and antibacterial effects [ 14 , 15 ]. A recent study has demonstrated that hesperidin protected cells against redox imbalances [ 16 ].…”