RETRACTED: Diosmetin exerts cardioprotective effect on myocardial ischaemia injury in neonatal rats by decreasing oxidative stress and myocardial apoptosis

Mo, Guo Liang; He, Yi; Zhang, Xiao Qian; Xia, Liangyu; Luo, Qi

doi:10.1111/1440-1681.13309

Cited by 24 publications

(17 citation statements)

References 40 publications

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“…A large number of pharmacological investigations have shown that diosmetin has anti-tumor, anti-acute kidney injury and anti-acute lung injury activities (Chen et al, 2019;Liu, Ci, Wen & Peng, 2018;Yang, Li, Yu, Yi & Huang, 2017). The previous studies also indicated that diosmetin can attenuate oxidative stress and decrease level of proinflammatory cytokine (Mo, He, Zhang, Lei & Luo, 2020;Zaragozá, Villaescusa, Monserrat, Zaragozá & Álvarez-Mon, 2020). In our experiment, we studied and reported the effects and potential molecular mechanisms of diosmetin treating IBD.…”

Section: Introductionmentioning

confidence: 79%

Potential pharmacological mechanism of Colitis treatment by diosmetin

Wei

et al. 2020

Preprint

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BACKGROUND AND PURPOSE Diosmetin exhibits a series of therapeutic efficacy but little is known of its effects on colitis. EXPERIMENTAL APPROACH In this study, two mouse models of DSS (the concentration of 3% and 5%)-induced colitis and Caco2 and IEC-6 cells were employed. The 16S amplicon sequencing was used to assess Gut microbiota changes by diosmetin. Various physical signs of mice (body weight, colon length and DAI score), proinflammatory cytokines and antioxidant enzymes were tested. KEY RESULTS The results showed that diosmetin can markedly decrease the disease activity index and microscopic colon tissue damage, increase the expression of tight junction protein (Occludin, Claudin-1 and Zo-1) and reduce the secretion of proinflammatory cytokines. And diosmetin also significantly inhibited colon oxidative damage through adjusting the levels of intracellular ROS, mitochondrial ROS, GSH-Px, SOD, MDA and GSH in vitro and in vivo. Furthermore, it was found that diosmetin can modulate the abundance of Bacteroidetes, Actinobacteria, Cyanobacteria and Firmicutes, which were reported to be the crucial bacteria related to inflammatory bowel disease (IBD). CONCLUSIONS AND IMPLICATIONS Our data suggested that diosmetin ameliorated the colitis in mice induced by DSS in the potential mechanism that it alleviates intestinal epithelial barrier damage, inhibits the secretion of proinflammatory cytokines, decreases oxidative stress and modulates gut microbiota. It implies that diosmetin may be a novel candidate to alleviate DSS-induced colitis or a lead compound for future optimization and modification.

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Section: Introductionmentioning

confidence: 79%

Potential pharmacological mechanism of Colitis treatment by diosmetin

Wei

et al. 2020

Preprint

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“…This has not always been the case, in sepsis-induced acute kidney injury (AKI), the expression of the Nrf2/HO-1 signal axis was enhanced after diosmetin treatment, which were reversed by siNrf2 [26]. In addition, diosmetin also showed cardioprotective effects in MI model neonatal rats, accompanied by a decrease in p-Nrf2/Nrf2 [27]. Diosmetin protects against LPS-induced acute lung injury (ALI) via increasing the expression of Nrf2 along with its target gene HO-1 and blocked the activation of NLRP3 inflammasome both in vivo and in vitro [28].…”

Section: Discussionmentioning

confidence: 99%

Diosmetin Protects against Cardiac Hypertrophy via p62/Keap1/Nrf2 Signaling Pathway

Guo

Cen

et al. 2022

Oxidative Medicine and Cellular Longevity

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An important pathophysiological consequence of pressure overload-induced cardiac hypertrophy is adverse cardiac remodeling, including structural changes in cardiomyocytes and extracellular matrix. Diosmetin (DIO), a monomethoxyflavone isolated from citrus fruits, had antioxidative stress effects in multiple organs. The purpose of this study was to examine the biological effect of diosmetin on pathological cardiac hypertrophy. In mice, diosmetin treatment reduced cardiac hypertrophy and dysfunction in an aortic banding- (AB-) induced pressure overload model and reducing myocardial oxidative stress by increasing antioxidant gene expression. In vitro, diosmetin (10 or 50 μm, 12 h or 24 h) protected PE-induced cardiomyocyte hypertrophy in neonatal rat cardiomyocytes. Mechanistically, diosmetin inhibited autophagy by activating the PI3K/Akt pathway. In particular, diosmetin induced the accumulation of p62 and its interaction with Keap1, promoted the nuclear translocation of Nrf2, and increased the expression of antioxidant stress genes in the process of cardiac hypertrophy. Furthermore, knockdown of p62 in rat primary cardiomyocytes abrogate the protective effect of diosmetin on cardiomyocyte hypertrophy. Similarly, the Nrf2 inhibitor ML385 obviously abolished the above effects by diosmetin treatment. In conclusion, our results suggest that diosmetin protects cardiac hypertrophy under pressure overload through the p62/Keap1/Nrf2 signaling pathway, suggesting the potential of diosmetin as a novel therapy for pathological cardiac hypertrophy.

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“…Reports suggest that a small dose of diosmetin protects against oxidative stress injury in myocardial ischaemia and inhibits cardiomyocyte apoptosis in rats. 29 Fifty rats were randomly allocated to five groups (10 rats/group):…”

Section: Dose Selection With Grouping and Treatmentmentioning

confidence: 99%

Diosmetin attenuate experimental ulcerative colitis in rats via suppression of NF-κB, TNF-α and IL-6 signalling pathways correlated with down-regulation of apoptotic events

Wang

2021

Eur J Inflamm

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Introduction Ulcerative colitis (UC) is a chronic inflammation of colon in which the innermost tissue of colon and rectum develops deep-rooted inflammation. Diosmetin is the aglycone of the flavonoid glycoside diosmin, commonly found in citrus fruits. Therapeutically diosmetin is indicated to demonstrate anticancer, antimicrobial, antioxidant, oestrogenic and anti-inflammatory activity. Methods In this research, we studied the action of diosmetin on TNBS (2,4,6-trinitrobenzene sulfonic acid)-induced UC in rats. Male Wister rats were anesthetised with pentobarbital and TNBS introduced by performing an enema. Diosmetin treatment was provided through oral gavage for the next 28 days. Animals were sacrificed on the 29th day and colon tissues were collected for further examinations. Results Diosmetin treatment decreased colonic ulceration dramatically and decreased the percentage of inflammation in the colonic mucosa. Depletion of the TNBS assisted of superoxide dismutase and catalase was substantially restricted, while lipid peroxidation was recorded in the colonic tissue as malondialdehyde content was also decreased. After treatment with diosmetin, the occurrence of TNF-α, IL-6and NF-κB was considerably lowered and the number of apoptotic cells observed was significantly reduced. Conclusion Taken together, these observations demonstrated the potential of diosmetin against ulcer formation and development.

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RETRACTED: Diosmetin exerts cardioprotective effect on myocardial ischaemia injury in neonatal rats by decreasing oxidative stress and myocardial apoptosis

Cited by 24 publications

References 40 publications

Potential pharmacological mechanism of Colitis treatment by diosmetin

Potential pharmacological mechanism of Colitis treatment by diosmetin

Diosmetin Protects against Cardiac Hypertrophy via p62/Keap1/Nrf2 Signaling Pathway

Diosmetin attenuate experimental ulcerative colitis in rats via suppression of NF-κB, TNF-α and IL-6 signalling pathways correlated with down-regulation of apoptotic events

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