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

Li, Shilai; Zhu, Jianmeng; Pan, Ling; Wan, Peiqi; Qin, Quanlin; Luo, Dianzhong; Pan, Wenhui; Wei, Yuqing; Xu, Yali; Shang, Liming; Ye, Xinping

doi:10.3892/etm.2021.10196

Cited by 4 publications

(2 citation statements)

References 43 publications

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“…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.…”

Section: Discussionmentioning

confidence: 99%

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

Gonçalves

Musskopf

Rivera-Concepcion

et al. 2022

IJMS

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This study aimed to evaluate the effects of hesperidin (HE) on in vitro osteoclastogenesis and dietary supplem entation on mouse periodontal disease and femoral bone phenotype. RAW 264.7 cells were stimulated with RANKL in the presence or absence of HE (1, 100 or 500 µM) for 5 days, and evaluated by TRAP, TUNEL and Western Blot (WB) analyses. In vivo, C57BL/6 mice were given HE via oral gavage (125, 250 and 500 mg/kg) for 4 weeks. A sterile silk ligature was placed between the first and second right maxillary molars for 10 days and microcomputed tomography (μCT), histopathological and immunohistochemical evaluation were performed. Femoral bones subjected or not to dietary HE (500 mg/kg) for 6 and 12 weeks were evaluated using μCT. In vitro, HE 500 µM reduced formation of RANKL-stimulated TRAP-positive(+) multinucleated cells (500 µM) as well as c-Fos and NFATc1 protein expression (p < 0.05), markers of osteoclasts. In vivo, dietary HE 500 mg/kg increased the alveolar bone resorption in ligated teeth (p < 0.05) and resulted in a significant increase in TRAP+ cells (p < 0.05). Gingival inflammatory infiltrate was greater in the HE 500 mg/kg group even in the absence of ligature. In femurs, HE 500 mg/kg protected trabecular and cortical bone mass at 6 weeks of treatment. In conclusion, HE impaired in vitro osteoclastogenesis, but on the contrary, oral administration of a high concentration of dietary HE increased osteoclast numbers and promoted inflammation-induced alveolar bone loss. However, HE at 500 mg/kg can promote a bone-sparing effect on skeletal bone under physiological conditions.

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Section: Discussionmentioning

confidence: 99%

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

Gonçalves

Musskopf

Rivera-Concepcion

et al. 2022

IJMS

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“…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 ].…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2022

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Particulate matter 2.5 (PM2.5) exposure can trigger adverse health outcomes in the human skin, such as skin aging, wrinkles, pigment spots, and atopic dermatitis. PM2.5 is associated with mitochondrial damage and the generation of reactive oxygen species (ROS). Hesperidin is a bioflavonoid that exhibits antioxidant and anti-inflammatory properties. This study aimed to determine the mechanism underlying the protective effect of hesperidin on human HaCaT keratinocytes against PM2.5-induced mitochondrial damage, cell cycle arrest, and cellular senescence. Human HaCaT keratinocytes were pre-treated with hesperidin and then treated with PM2.5. Hesperidin attenuated PM2.5-induced mitochondrial and DNA damage, G0/G1 cell cycle arrest, and SA-βGal activity, the protein levels of cell cycle regulators, and matrix metalloproteinases (MMPs). Moreover, treatment with a specific c-Jun N-terminal kinase (JNK) inhibitor, SP600125, along with hesperidin markedly restored PM2.5-induced cell cycle arrest and cellular senescence. In addition, hesperidin significantly reduced the activation of MMPs, including MMP-1, MMP-2, and MMP-9, by inhibiting the activation of activator protein 1. In conclusion, hesperidin ameliorates PM2.5-induced mitochondrial damage, cell cycle arrest, and cellular senescence in human HaCaT keratinocytes via the ROS/JNK pathway.

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The protective effect of hesperidin on the liver of hypothyroid rats mediated by nuclear factor erythroid 2-related factor 2-dependent activation of heme oxygenase 1

et al. 2022

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

Cited by 4 publications

References 43 publications

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

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

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

The protective effect of hesperidin on the liver of hypothyroid rats mediated by nuclear factor erythroid 2-related factor 2-dependent activation of heme oxygenase 1

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