Antioxidant activity and inhibition effect on the growth of human colon carcinoma (HT-29) cells of esculetin from Cortex Fraxini

Wang, Kai; Zhang, Ye; Ekunwe, Stephen I.N.; Yi, Xianghui; Liu, Xianxian; Wang, Hengshan; Pan, Ying‐Ming

doi:10.1007/s00044-010-9426-y

Cited by 18 publications

(14 citation statements)

References 30 publications

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“…Our results are agreement with several previous findings in which esculetin is a potential naturally occurring antioxidant both in vitro and in vivo [36,37]. Probably, the anti-oxidant effect of esculetin could by hydrogen donating ability of esculetin [38], the catechol structure of esculetin contributes the stronger antioxidant activity [36]. The available data of the present study confirms with existing literature that, esculetin has the ability to activate anti-oxidant enzymes or and might combat the excess ROS formed with in the cell [39,40].…”

Section: Discussionsupporting

confidence: 93%

Exploring cardioprotective potential of esculetin against isoproterenol induced myocardial toxicity in rats: in vivo and in vitro evidence

Pullaiah

Nelson

Rayapu

et al. 2021

BMC Pharmacol Toxicol

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Background Esculetin is a natural coumarin derivative from various plants with multiple pharmacological effects. Hence, the present study was undertaken to explore the cardio protective potential of esculetin against isoproterenol induced myocardial toxicity in rats. Methods The treatment schedule was fixed for 28 days and the rats were divided into five groups of six each. Rats of group I received the normal saline and served as normal control, group II was received ISO (100 mg/kg body weight) for last two consecutive days of the study and served as disease control. Groups III and IV received esculetin 10 and 20 mg/kg body weight respectively once a day per oral for 28 days along with ISO for last two consecutive days of the study. Cardiac biomarkers such as CK-MB and LDH, membrane bound Na+ /K+ ATPases activity, myocardial lysosomal enzymes activity and tissue antioxidants status were estimated in the heart tissue samples. The histopathological changes in the myocardium were also assessed. Further, DPPH assay was done to evaluate the free radicals scavenging potential of esculetin. Cytoxicity assay, intracellular ROS levels by DCFDA assay and m-RNA expression of TNF-α, IL-6 and NF-κB by quantitative RT-PCR in H9c2 cell lines. Results The increased levels of CK-MB, LDH, LPO, myocardial lysosomal enzymes and membrane bound Na+ /K+ ATPase levels by ISO administration was significantly increased with concomitant decrease in tissue antioxidant enzymes such as GSH, Catalase, and SOD. Pre-treatment with esculetin for 28 days has significantly decreased the levels of cardiac bio-markers, lysosomal enzymes, membrane bound Na+ /K+ ATPase levels as well as Lipid peroxides which is in contrary to the ISO group. Amelioration of the antioxidant levels were also found in esculetin treated groups. Histopathological examination of heart reveals that myocardial degeneration, mononuclear cell infiltration was noticed in ISO treated rats, whereas the same was restored with esculetin treatment. In H9C2 cell lines esculetin could effectively reduced intracellular ROS inhibition and m-RNA expression of pro-inflammatory cytokines including TNF-α, IL-6 and NF-κB to prevent apoptosis or cell necrosis. Conclusion The study provides the evidence of cardioprotective potentials of esculetin against isoproterenol induced myocardial infarction by antioxidant and myocardial membrane stabilization along with in vitro protection from arsenic induced ROS cell necrosis or apoptosis in H9C2 cells.

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Section: Discussionsupporting

confidence: 93%

Exploring cardioprotective potential of esculetin against isoproterenol induced myocardial toxicity in rats: in vivo and in vitro evidence

Pullaiah

Nelson

Rayapu

et al. 2021

BMC Pharmacol Toxicol

View full text Add to dashboard Cite

show abstract

“…Probably, the anti-oxidant effect of esculetin could by hydrogen donating ability of esculetin [38], the catechol structure of esculetin contributes the stronger antioxidant activity [36]. The available data of the present study con rms with existing literature that, esculetin has the ability to activate anti-oxidant enzymes or and might combat the excess ROS formed with in the cell [39,40].…”

Section: Discussionsupporting

confidence: 79%

Exploring Cardioprotective Potential of Esculetin Against Isoproterenol Induced Myocardial Infarction in Rats: In Vivo and in Vitro Evidence

Pullaiah

Nelson²,

Sushma

et al. 2021

Preprint

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BackgroundEsculetin is a natural coumarin derivative from various plants with multiple pharmacological effects. Hence, the present study was undertaken to explore the cardio protective potential of esculetin against isoproterenol induced myocardial toxicity in rats. Methods The treatment schedule was fixed for 28 days and the rats were divided into five groups of six each. Rats of group I received the normal saline and served as normal control, group II was received ISO (100mg/kg body weight) for last two consecutive days of the study and served as disease control. Groups III and IV received esculetin 10 and 20 mg/kg body weight respectively once a day per oral for 28 days along with ISO for last two consecutive days of the study. Cardiac biomarkers such as CK-MB and LDH, membrane bound Na+ /K+ ATPases activity, myocardial lysosomal enzymes activity and tissue antioxidants status were estimated in the heart tissue samples. The histopathological changes in the myocardium were also assessed. Further, DPPH assay was done to evaluate the free radicals scavenging potential of esculetin. Cytoxicity assay, intracellular ROS levels by DCFDA assay and m-RNA expression of TNF-α, IL-6 and NF-κB by quantitative RT-PCR in H9c2 cell lines.ResultsThe increased levels of CK-MB, LDH, LPO, myocardial lysosomal enzymes and membrane bound Na+ /K+ ATPase levels by ISO administration was significantly increased with concomitant decrease in tissue antioxidant enzymes such as GSH, Catalase, and SOD. Pre-treatment with esculetin for 28 days has significantly decreased the levels of cardiac bio-markers, lysosomal enzymes, membrane bound Na+ /K+ ATPase levels as well as Lipid peroxides which is in contrary to the ISO group. Amelioration of the antioxidant levels were also found in esculetin treated groups. Histopathological examination of heart reveals that myocardial degeneration, mononuclear cell infiltration was noticed in ISO treated rats, whereas the same was restored with esculetin treatment. In H9C2 cell lines esculetin could effectively reduced intracellular ROS inhibition and m-RNA expression of pro-inflammatory cytokines including TNF-α, IL-6 and NF-κB to prevent apoptosis or cell necrosis. Conclusion The study provides the evidence of cardioprotective potentials of esculetin against isoproterenol induced myocardial infarction by antioxidant and myocardial membrane stabilization along with in vitro protection from arsenic induced ROS cell necrosis or apoptosis in H9C2 cells.

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“…Cortex Fraxini, the dried bark of F. rhynchophylla Hance, has a variety of biological activities, including antioxidant, anticancer, anti-inflammatory, and photo-protective effects [ 18 , 19 , 20 , 21 ]. A large number of coumarins exhibit anti-inflammatory properties, including isofraxidin, which inhibits TNF-α production by LPS-induced mouse peritoneal macrophages via the MAPK pathway [ 22 ]; IMM-H004, which attenuates the production of inflammatory mediators in LPS-stimulated BV2 microglia [ 23 ]; and psoralidin, which inhibits LPS-induced iNOS expression by repressing Syk-mediated activation of PI3K-IKK-IκB signaling pathways [ 24 ].…”

Section: Resultsmentioning

confidence: 99%

5-Methoxyl Aesculetin Abrogates Lipopolysaccharide-Induced Inflammation by Suppressing MAPK and AP-1 Pathways in RAW 264.7 Cells

Long

et al. 2016

IJMS

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For the first time, a pale amorphous coumarin derivative, 5-methoxyl aesculetin (MOA), was isolated from the dried bark of Fraxinus rhynchophylla Hance (Oleaceae). MOA modulates cytokine expression in lipopolysaccharide (LPS)-treated RAW 264.7 macrophages, but the precise mechanisms are still not fully understood. We determined the effects of MOA on the production of inflammatory mediators and pro-inflammatory cytokines in the LPS-induced inflammatory responses of RAW 264.7 macrophages. MOA significantly inhibited the LPS-induced production of nitric oxide (NO), prostaglandin E2 (PGE2), tumor necrosis factor-α (TNF-α), interleukin-6, and interleukin-1β. It also effectively attenuated inducible nitric oxide (NO) synthase, cyclooxygenase-2, and TNF-α mRNA expression and significantly decreased the levels of intracellular reactive oxygen species. It inhibited phosphorylation of the extracellular signal-regulated kinase (ERK1/2), thus blocking nuclear translocation of activation protein (AP)-1. In a molecular docking study, MOA was shown to target the binding site of ERK via the formation of three hydrogen bonds with two residues of the kinase, which is sufficient for the inhibition of ERK. These results suggest that the anti-inflammatory effects of MOA in RAW 264.7 macrophages derive from its ability to block both the activation of mitogen-activated protein kinases (MAPKs) and one of their downstream transcription factors, activator protein-1 (AP-1). Our observations support the need for further research into MOA as a promising therapeutic agent in inflammatory diseases.

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Antioxidant activity and inhibition effect on the growth of human colon carcinoma (HT-29) cells of esculetin from Cortex Fraxini

Cited by 18 publications

References 30 publications

Exploring cardioprotective potential of esculetin against isoproterenol induced myocardial toxicity in rats: in vivo and in vitro evidence

Exploring cardioprotective potential of esculetin against isoproterenol induced myocardial toxicity in rats: in vivo and in vitro evidence

Exploring Cardioprotective Potential of Esculetin Against Isoproterenol Induced Myocardial Infarction in Rats: In Vivo and in Vitro Evidence

5-Methoxyl Aesculetin Abrogates Lipopolysaccharide-Induced Inflammation by Suppressing MAPK and AP-1 Pathways in RAW 264.7 Cells

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