scholarly journals Antioxidative and Cardioprotective Effects of Schisandra chinensis Bee Pollen Extract on Isoprenaline-Induced Myocardial Infarction in Rats

Molecules ◽  
2019 ◽  
Vol 24 (6) ◽  
pp. 1090 ◽  
Author(s):  
Zhenhuang Shen ◽  
Qianqian Geng ◽  
Haibo Huang ◽  
Hong Yao ◽  
Tianyu Du ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Scientific Basis ◽  
Heme Oxygenase 1 ◽  
Pollen Extract ◽  
Related Factor ◽  
Schisandra Chinensis ◽  
Model Group ◽  
Bee Pollen ◽  
Cardioprotective Effects ◽  
High Doses

Oxidative stress plays an important role in the pathogenesis of myocardial infarction (MI). Schisandra chinensis bee pollen extract (SCBPE) possesses powerful antioxidant capacity. This study aimed to further explore the antioxidative and cardioprotective effects of SCBPE on acute MI induced by isoprenaline (ISO) in rats. The rats were intragastrically administrated with SCBPE (600, 1200, or 1800 mg/kg/day) and Compound Danshen dropping pills (270 mg/kg/day) for 30 days, then subcutaneously injected with ISO (65 mg/kg/day) on the 29th and 30th day. Compared with the model group, pretreatment with middle and high doses of SCBPE significantly reduced serum aspartate transaminase, lactate dehydrogenase, and creatine kinase activities and increased myocardial superoxide dismutase, glutathione peroxidase, and catalase activities. The histopathologic aspects showed that pathological heart change was found in the model group and reduced to varying degrees in the SCBPE groups. Moreover, the protein expression of nuclear factor-erythroid 2-related factor 2 (Nrf-2), heme oxygenase-1 (HO-1), and Bcl2 in the heart increased in the SCBPE groups, while that of Bax decreased compared to the model group. Besides this, uridine was isolated from S. chinensis bee pollen for the first time. This study could provide a scientific basis for using Schisandra chinensis bee pollen as a functional food for the prevention of MI.

Protective effect of Schisandra chinensis bee pollen extract on liver and kidney injury induced by cisplatin in rats

2017 ◽  
Vol 95 ◽  
pp. 1765-1776 ◽  
Author(s):  
Haibo Huang ◽  
Zhenhuang Shen ◽  
Qianqian Geng ◽  
Zhenhong Wu ◽  
Peiying Shi ◽  
...  
Keyword(s):  
Protective Effect ◽  
Kidney Injury ◽  
Pollen Extract ◽  
Schisandra Chinensis ◽  
Bee Pollen ◽  
Liver And Kidney

Effect of Noni on memory impairment induced by hydrocortisone in mice

2021 ◽  
Author(s):  
RUI ZHANG ◽  
JINLIAN LIU ◽  
XINJUAN HOU ◽  
FAN ZHAO ◽  
CHANDI WANG ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Memory Impairment ◽  
Control Group ◽  
Heme Oxygenase 1 ◽  
High Dose ◽  
Related Factor ◽  
Model Group ◽  
Protection Mechanism ◽  
Protein Expressions ◽  
Biochemical Analyses

Abstract Background Oxidative stress and memory impairment have been implicated, a common functional brain disease. Nuclear factor E2-related factor 2 (Nrf2) is highly induced in oxidative stress, indicating that Nrf2 is an emerging target of memory therapy. This study aimed to investigate the effect of Noni on brain memory impairment induced by hydrocortisone and its protection mechanism in mice. Methods Male Kuming mice were (n = 8/group) given hydrocortisone by gastric gavage for 14 consecutive days to establish the memory impairment model except for those in the control group. At the same day, the corresponding drugs were given by gastric gavage. The changes in ethology were examined. Brains were extracted and subjected to western blot analysis and biochemical analyses to assess the activities of oxidative stress. Results The middle and high-dose Noni groups ameliorated the ethology and the high-dose Noni group increased cerebral protein expressions of Nrf2, kelch-like ECH-associated protein 1 (KEAP1) and heme oxygenase-1 (HO-1), as compared to the model group. The arrangement of CA3 vertebral cells in hippocampus of mice was slightly compact and hyperchromatic and pyknosis were alleviated. Furthermore, the biochemical analyses showed the activities of related enzymes of oxidative stress in high-dose Noni group were increased. Conclusions Noni might be a powerful antioxidant that can protect nerve cell and may possess as a potential benefit for the treatment of memory impairment.

Saponins from Panax japonicas Reduces Myocardial Infarction Induced Reactive Oxygen Species Production and Cardiomyocyte Apoptosis via Activation of the Nrf-2 Pathway

2014 ◽  
Vol 881-883 ◽  
pp. 339-346 ◽  
Author(s):  
Na Wei ◽  
Ding Yuan ◽  
Hai Bo He ◽  
Yuan Qing Xu ◽  
Chang Cheng Zhang ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Reactive Oxygen Species ◽  
Antioxidant Properties ◽  
Reactive Oxygen ◽  
Cardiomyocyte Apoptosis ◽  
Related Factor ◽  
Oxygen Species ◽  
Anti Oxidant ◽  
Cardioprotective Effects ◽  
Species Production

Myocardial infarction (MI) increased reactive oxygen species (ROS) and cardiomyocyte apoptosis. Saponins fromPanax japonicus(SPJ) exerted beneficially cardioprotective effects on myocardial ischemia injury and possess antioxidant properties to scavenge the toxic radicals. Nuclear factor erythroid 2-related factor (Nrf2) is a transcription factor that controls the expression of a large pool of anti-oxidant and protects cells from oxidative damage. The data from this study show that SPJ reduced the production of ROS by increase the expression of antioxidants and restore the balance between prooxidants and antioxidants via activation of the Nrf-2 pathway. Furthermore, SPJ might reduce ROS production and apoptosis in hydrogen peroxide-induced H9c2 cells. The effect of MI apoptotic cells induces generation of ROS in abundance. Taken together, SPJ treatment significantly improved MI-induced injury and this may be attributing to inhibiting ROS related apoptosis via activation of the Nrf-2 pathway.

scholarly journals Phikud Navakot Modulates the Level of Pro-Inflammatory Mediators and the Protein Expression of SOD1 and 2 and the Nrf2/HO-1 Signaling Pathway in Rats with Acute Myocardial Infarction

2019 ◽  
Vol 2019 ◽  
pp. 1-13
Author(s):  
Orapin Gerdprasert ◽  
Nantana Choomchuay ◽  
Boonrat Chantong ◽  
Narueporn Sutanthavibul ◽  
Duangdeun Meksuriyen ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Troponin T ◽  
Antioxidant Properties ◽  
Ethanolic Extract ◽  
Inflammatory Cells ◽  
Related Factor ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
St Segment ◽  
Cardioprotective Effects

Phikud Navakot (PN) is nine major herbs in a famous traditional Thai recipe namely “Yahom Navakot” used to treat cardiovascular disorders. This study investigated the cardioprotective effects of PN formula on isoproterenol-induced myocardial infarction (IMI) in Sprague-Dawley rats. Forty-five rats were randomly divided into nine groups (n = 5 per group): the control, the IMI, the IMI + propranolol, the control or the IMI + PN formula (PN ethanolic extract at doses of 64, 127, or 255 mg/kg) by oroesophageal gavage for 28 days. The ST segment and serum troponin T levels were significantly increased in IMI rats. PN did not eliminate tissue necrosis, infiltration of inflammatory cells, or interstitial edema in IMI rats. All doses of PN decreased (p<0.001) serum TNF-α and IL-6 levels. PN (127 and 255 mg/kg) up-regulated (p<0.05) heme oxygenase (HO)-1 expression, whereas PN (255 mg/kg) significantly increased superoxide dismutase (SOD) 1 and 2 expression, compared with IMI rats. Nuclear factor erythroid 2-related factor 2 (Nrf2) and HO-1 expression significantly increased in IMI rats and IMI rats that received PN. PN formula possesses potential anti-inflammatory and antioxidant properties by modulating the levels of TNF-α, IL-6 and antioxidant enzymes. Our study reveals a novel cardioprotective effect of PN in IMI rats through the Nrf2/HO-1 signaling.

Preinfarction Angina and Improved Reperfusion of the Infarct-related Artery

1999 ◽  
Vol 82 (S 01) ◽  
pp. 68-72 ◽  
Author(s):  
Alessandro Sciahbasi ◽  
Eugenia De Marco ◽  
Attilio Maseri ◽  
Felicita Andreotti
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Infarct Size ◽  
Ischemic Preconditioning ◽  
Early Reperfusion ◽  
Vast Number ◽  
Beneficial Effects ◽  
Infarct Related Artery ◽  
Cardioprotective Effects ◽  
Collateral Vessels

SummaryPreinfarction angina and early reperfusion of the infarct-related artery are major determinants of reduced infarct-size in patients with acute myocardial infarction. The beneficial effects of preinfarction angina on infarct size have been attributed to the development of collateral vessels and/or to post-ischemic myocardial protection. However, recently, a relation has been found between prodromal angina, faster coronary recanalization, and smaller infarcts in patients treated with rt-PA: those with preinfarction angina showed earlier reperfusion (p = 0.006) and a 50% reduction of CKMB-estimated infarct-size (p = 0.009) compared to patients without preinfarction angina. This intriguing observation is consistent with a subsequent observation of higher coronary recanalization rates following thrombolysis in patients with prodromal preinfarction angina compared to patients without antecedent angina. Recent findings in dogs show an enhanced spontaneous lysis of plateletrich coronary thrombi with ischemic preconditioning, which is prevented by adenosine blockade, suggesting an antithrom-botic effect of ischemic metabolites. Understanding the mechanisms responsible for earlier and enhanced coronary recanalization in patients with preinfarction angina may open the way to new reperfusion strategies.A vast number of studies, globally involving ≈17,000 patients with acute myocardial infarction, have unequivocally shown that an infarction preceded by angina evolves into a smaller area of necrosis compared to an infarct not preceded by angina (Table 1) (1). So far, preinfarction angina has been thought to have cardioprotective effects mainly through two mechanisms: collateral perfusion of the infarctzone (2-4), and ischemic preconditioning of the myocardium (5-7). Here we discuss a further mechanism of protection represented by improved reperfusion of the infarct-related artery.

Trilobatin Protects Cardiomyocytes from Hypoxia/ Reperfusion Injury by Regulating the Nuclear Factor Erythroid 2-Related Factor 2/Heme Oxygenase-1 Pathway

2020 ◽  
Vol 19 (2) ◽  
pp. 133-138
Author(s):  
Wenyu Chen ◽  
Hui He
Keyword(s):  
Heme Oxygenase ◽  
Molecular Mechanisms ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Cellular Injury ◽  
Nuclear Factor ◽  
Oxygen Species ◽  
H9c2 Cells ◽  
Natural Plant ◽  
Induced Changes

Trilobatin is a natural plant-derived glycosylated flavonoid that has been shown to exhibit multiple beneficial pharmacologic activities including protection of heart against H/R-induced cardiomyocyte injury. However, the molecular mechanisms underlying protection from H/R-induced cardiomyocyte injury remain unknown. Using H9C2 cells as a model, we examined the effect of trilobatin on H/R-induced cellular injury, apoptosis, and generation of reactive oxygen species. The results showed that trilobatin protected H9C2 cells not only from cell death and apoptosis, but also counteracted H/R-induced changes in malondialdehyde, superoxide dismutase, glutathione, and glutathione peroxidase. The evaluation of the mechanism underlying the effect of trilobatin on protection from H/R-induced cellular injury suggested changes in the regulation of nuclear factor erythroid 2-related factor 2/heme oxygenase-1 pathway.

Therapeutic Potential of Biochanin-A Against Isoproterenol-Induced Myocardial Infarction in Rats

2020 ◽  
Vol 18 (1) ◽  
pp. 31-36 ◽  
Author(s):  
Sangeethadevi Govindasami ◽  
Veera Venkata Sathibabu Uddandrao ◽  
Nivedha Raveendran ◽  
Vadivukkarasi Sasikumar
Keyword(s):  
Myocardial Infarction ◽  
Antioxidant Enzymes ◽  
Therapeutic Potential ◽  
Biochanin A ◽  
Glutathione S Transferase ◽  
Serum Glutamic Oxaloacetic Transaminase ◽  
Creatine Kinase Mb ◽  
Male Wistar Rats ◽  
Detoxifying Enzyme ◽  
Cardioprotective Effects

Background: This study determined the effect of Biochanin A (BCA) on isoproterenol (ISO) induced Myocardial Infarction (MI) in male Wistar rats. Methods: Animals (weighing 150-180 g) were divided into four groups, with six animals in each group and pretreated with BCA (10mg/kg Body Weight [BW]) and ɑ-tocopherol (60mg/kg BW) for 30 days; and ISO (20mg/kg BW) was administrated subcutaneously on the 31st and 32nd day. Results: ISO-induced MI rats demonstrated the significant elevation of serum glutamic oxaloacetic transaminase, serum glutamic pyruvic transaminase, lactate dehydrogenase, creatine kinase-MB and cardiac troponin; however, concomitant pretreatment with BCA protected the rats from cardiotoxicity caused by ISO. Activities of antioxidant enzymes, such as superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase and glutathione reductase significantly reduced in the heart with ISO-induced MI. Pretreatment with BCA produced a marked reversal of these antioxidant enzymes related to MI-induced by ISO. Conclusion: In conclusion, this study suggested that BCA exerts cardioprotective effects through modulating lipid peroxidation, enhancing antioxidants, and detoxifying enzyme systems.

scholarly journals Heme-Mediated Activation of the Nrf2/HO-1 Axis Attenuates Calcification of Valve Interstitial Cells

Biomedicines ◽  
2021 ◽  
Vol 9 (4) ◽  
pp. 427
Author(s):  
Enikő Balogh ◽  
Arpan Chowdhury ◽  
Haneen Ababneh ◽  
Dávid Máté Csiki ◽  
Andrea Tóth ◽  
...  
Keyword(s):  
Target Gene ◽  
Interstitial Cells ◽  
Protective Role ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Valvular Interstitial Cells ◽  
Aortic Valves ◽  
Antioxidant Genes ◽  
Valve Interstitial Cells ◽  
Nrf2 Target Gene

Calcific aortic valve stenosis (CAVS) is a heart disease characterized by the progressive fibro-calcific remodeling of the aortic valves, an actively regulated process with the involvement of the reactive oxygen species-mediated differentiation of valvular interstitial cells (VICs) into osteoblast-like cells. Nuclear factor erythroid 2-related factor 2 (Nrf2) regulates the expression of a variety of antioxidant genes, and plays a protective role in valve calcification. Heme oxygenase-1 (HO-1), an Nrf2-target gene, is upregulated in human calcified aortic valves. Therefore, we investigated the effect of Nrf2/HO-1 axis in VIC calcification. We induced osteogenic differentiation of human VICs with elevated phosphate and calcium-containing osteogenic medium (OM) in the presence of heme. Heme inhibited Ca deposition and OM-induced increase in alkaline phosphatase and osteocalcin (OCN) expression. Heme induced Nrf2 and HO-1 expression in VICs. Heme lost its anti-calcification potential when we blocked transcriptional activity Nrf2 or enzyme activity of HO-1. The heme catabolism products bilirubin, carbon monoxide, and iron, and also ferritin inhibited OM-induced Ca deposition and OCN expression in VICs. This study suggests that heme-mediated activation of the Nrf2/HO-1 pathway inhibits the calcification of VICs. The anti-calcification effect of heme is attributed to the end products of HO-1-catalyzed heme degradation and ferritin.

scholarly journals Sanghuangporus sanghuang Mycelium Prevents Paracetamol-Induced Hepatotoxicity through Regulating the MAPK/NF-κB, Keap1/Nrf2/HO-1, TLR4/PI3K/Akt and CaMKKβ/LKB1/AMPK Pathways and Suppressing Oxidative Stress and Inflammation

Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 897
Author(s):  
Wen-Ping Jiang ◽  
Jeng-Shyan Deng ◽  
Shyh-Shyun Huang ◽  
Sheng-Hua Wu ◽  
Chin-Chu Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protein Kinase ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Mitogen Activated Protein Kinase ◽  
Heme Oxygenase 1 ◽  
Molecular Evidence ◽  
Related Factor ◽  
Serum Aminotransferase ◽  
Compound C

Liver damage induced by paracetamol overdose is the main cause of acute liver failure worldwide. In order to study the hepatoprotective effect of Sanghuangporus sanghuang mycelium (SS) on paracetamol-induced liver injury, SS was administered orally every day for 6 days in mice before paracetamol treatment. SS decreased serum aminotransferase activities and the lipid profiles, protecting against paracetamol hepatotoxicity in mice. Furthermore, SS inhibited the lipid peroxidation marker malondialdehyde (MDA), hepatic cytochrome P450 2E1 (CYP2E1), and the histopathological changes in the liver and decreased inflammatory activity by inhibiting the production of proinflammatory cytokines in paracetamol-induced acute liver failure. Moreover, SS improved the levels of glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase in the liver. Significantly, SS diminished mitogen-activated protein kinase (MAPK), Toll-like receptor 4 (TLR4), phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt), and the nuclear factor-kappa B (NF-κB) axis, as well as upregulated the Kelch-like ECH-associated protein 1 (Keap1)/erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway, in paracetamol-induced mice. SS mainly inhibited the phosphorylation of the liver kinase B1 (LKB1), Ca2+/calmodulin-dependent kinase kinase β (CaMKKβ), and AMP-activated protein kinase (AMPK) protein expression. Furthermore, the protective effects of SS on paracetamol-induced hepatotoxicity were abolished by compound C, an AMPK inhibitor. In summary, we provide novel molecular evidence that SS protects liver cells from paracetamol-induced hepatotoxicity by inhibiting oxidative stress and inflammation.

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