Myocardial Ischemia https://greenmedinfo.com/taxonomy/term/2408/all en Chrysin rescues rat myocardium from ischemia-reperfusion injury via PPAR-γ/Nrf2 activation. https://greenmedinfo.com/article/chrysin-rescues-rat-myocardium-ischemia-reperfusion-injury-ppar-nrf2-activatio PMID:  Eur J Pharmacol. 2020 Jul 22 ;883:173389. Epub 2020 Jul 22. PMID: 32707190 Abstract Title:  Chrysin rescues rat myocardium from ischemia-reperfusion injury via PPAR-γ/Nrf2 activation. Abstract:  Pharmacological strategies aimed at co-activating peroxisome proliferator-activated receptor-gamma (PPAR-γ)/nuclear factor erythroid 2-related factor 2 (Nrf2) pathway have shown promising results in alleviating myocardial injury. The aim of the study was to evaluate the role of chrysin, a PPAR-γ agonist, in ischemia-reperfusion (IR)-induced myocardial infarction (MI) in rats and to explore the molecular mechanism driving this activity. To evaluate this hypothesis, chrysin (60 mg/kg, orally), PPAR-γ antagonist (GW9662, 1 mg/kg, intraperitoneally), or both were administered to rats for 28 days. On the 29th day, one-stage ligation of left anterior descending coronary artery for 45 min followedby 60 min of reperfusion was performed. Chrysin significantly decreased infarct size and improved cardiac functions following IR-induced MI. This improvement was corroborated by augmented PPAR-γ/Nrf2 expression as confirmed by immunohistochemistry and western blotting analysis. Chrysin exhibitedstrong anti-oxidant property as demonstrated by increased GSH and CAT levels and decreased 8-OHdG and TBARS levels. Our findings also imply that chrysin significantly inhibited inflammatory response as validated by decreased NF-κB, IKK-β, CRP, TNF-α and MPO levels. In addition, chrysin decreasedTUNEL/DAPI positivity, a marker of apoptotic response and normalized cardiac injury markers. The histopathological and ultrastructural analysis further supported the functional and biochemical outcomes, showing preserved myocardial architecture. Intriguingly, co-administration with GW9662 significantly diminished the cardioprotective effect of chrysin as demonstrated by depressed myocardial function, decreased PPAR-γ/Nrf2 expression and increased oxidative stress. In conclusion, the present study demonstrates that co-activation of PPAR-γ/Nrf2 by chrysin may be crucial for its cardioprotective effect. <p><a href="https://greenmedinfo.com/article/chrysin-rescues-rat-myocardium-ischemia-reperfusion-injury-ppar-nrf2-activatio" target="_blank">read more</a></p> https://greenmedinfo.com/article/chrysin-rescues-rat-myocardium-ischemia-reperfusion-injury-ppar-nrf2-activatio#comments Chrysin Myocardial Ischemia Cardioprotective Animal Study Wed, 12 Aug 2020 21:43:34 +0000 greenmedinfo 225132 at https://greenmedinfo.com Electroacupuncture improves myocardial ischemia injury via activation of adenosine receptors. https://greenmedinfo.com/article/electroacupuncture-improves-myocardial-ischemia-injury-activation-adenosine-re PMID:  Purinergic Signal. 2020 Jul 6. Epub 2020 Jul 6. PMID: 32632520 Abstract Title:  Electroacupuncture improves myocardial ischemia injury via activation of adenosine receptors. Abstract:  Electroacupuncture (EA) can improve myocardial ischemia (MI) injury; nevertheless, the mechanism is not entirely clear. And there were disagreements about whether the effect of EA at acupoint in disease-affected meridian is better than EA at acupoint in non-affected meridian and sham acupoint. Here, we showed that the effect of EA at Neiguan (PC6) is better than EA at Hegu (LI4) and sham acupoint in affecting RPP and ECG, increasing ATP and ADO production, decreasing AMP production, and upregulating the mRNA expression levels of A1AR, A2aAR, and A2bAR; knockdown of A1AR or A2bAR reversed the effect of EA at PC6 in alleviating MI injury; knockdown of A2aAR had no influence on the cardiac protection of EA at PC6; thus, the cardioprotective effect of EA at PC6 needs A1AR and A2bAR, instead of A2aAR; considering that the cardio protection of adenosine receptor needs activation of other adenosine receptors, one of the reasons may be that after silence of A1AR or A2bAR, EA at PC6 could not impact the expression levels of the other two adenosine receptors, and after silence of A2aAR, EA at PC6 could impact the expression levels of A1AR and A2bAR. These results suggested that EA at PC6 may be a potential and effective treatment for MI by activation of A1AR and A2bAR. <p><a href="https://greenmedinfo.com/article/electroacupuncture-improves-myocardial-ischemia-injury-activation-adenosine-re" target="_blank">read more</a></p> https://greenmedinfo.com/article/electroacupuncture-improves-myocardial-ischemia-injury-activation-adenosine-re#comments Myocardial Ischemia Cardioprotective Electroacupuncture Animal Study Wed, 22 Jul 2020 12:19:33 +0000 greenmedinfo 223975 at https://greenmedinfo.com Piperlonguminine a new mitochondrial aldehyde dehydrogenase activator protects the heart from ischemia/reperfusion injury. https://greenmedinfo.com/article/piperlonguminine-new-mitochondrial-aldehyde-dehydrogenase-activator-protects-h PMID:  Biochim Biophys Acta Gen Subj. 2020 Nov ;1864(11):129684. Epub 2020 Jul 14. PMID: 32679250 Abstract Title:  Piperlonguminine a new mitochondrial aldehyde dehydrogenase activator protects the heart from ischemia/reperfusion injury. Abstract:  BACKGROUND: Detoxification of aldehydes by aldehyde dehydrogenases (ALDHs) is crucial to maintain cell function. In cardiovascular diseases, reactive oxygen species generated during ischemia/reperfusion events trigger lipoperoxidation, promoting cell accumulation of highly toxic lipid aldehydes compromising cardiac function. In this context, activation of ALDH2, may contribute to preservation of cell integrity by diminishing aldehydes content more efficiently.METHODS: The theoretic interaction of piperlonguminine (PPLG) with ALDH2 was evaluated by docking analysis. Recombinant human ALDH2 was used to evaluate the effects of PPLG on the kinetics of the enzyme. The effects of PPLG were further investigated in a myocardial infarction model in rats, evaluating ALDHs activity, antioxidant enzymes, oxidative stress markers and mitochondrial function.RESULTS: PPLG increased the activity of recombinant human ALDH2 and protected the enzyme from inactivation by lipid aldehydes. Additionally, administration of this drug prevented the damage induced by ischemia/reperfusion in rats, restoring heart rate and blood pressure, which correlated with protection of ALDHs activity in the tissue, a lower content of lipid aldehydes, and the preservation of mitochondrial function.CONCLUSION: Activation of ALDH2 by piperlonguminine ameliorates cell damage generated in heart ischemia/reperfusion events, by decreasing lipid aldehydes concentration promoting cardioprotection. <p><a href="https://greenmedinfo.com/article/piperlonguminine-new-mitochondrial-aldehyde-dehydrogenase-activator-protects-h" target="_blank">read more</a></p> https://greenmedinfo.com/article/piperlonguminine-new-mitochondrial-aldehyde-dehydrogenase-activator-protects-h#comments Myocardial Ischemia Piperlongumine Cardioprotective In Vitro Study Fri, 04 Sep 2020 20:34:08 +0000 greenmedinfo 226308 at https://greenmedinfo.com The Advances on the protective effects of ginsenosides on myocardial ischemia and ischemia-reperfusion injury. https://greenmedinfo.com/article/advances-protective-effects-ginsenosides-myocardial-ischemia-and-ischemia-repe PMID:  Mini Rev Med Chem. 2020 Jun 19. Epub 2020 Jun 19. PMID: 32560603 Abstract Title:  The Advances on the protective effects of ginsenosides on myocardial ischemia and ischemia-reperfusion injury. Abstract:  Ginseng is a traditional medicine with a complex chemical composition, wide bioactivity and unique pharmacological action. Many studies have confirmed that ginsenosides are the active ingredients of ginseng, and ginsenosides have always been the focus of different researchers. With the development of modern separation and analysis technology, more than 150 kinds of ginsenosides have been isolated. The ginsenosides Rb1, Rb2, Rc, Rg1 and Re account for more than 80% of total ginsenosides, and other saponins, such as Rd, Rg3 and Rh2, which are minor constituents, account for only a small portion of the total amount. In recent years, ginsenosides have been found to possess strong pharmacological activities, such as antioxidation, clearing of oxygen free radicals, reducing calcium overload and anti-apoptosis. Ginsenosides play a protective role in ischemia-reperfusion injury. This paper reviews the protective effects of ginsenosides on myocardial ischemia and ischemia-reperfusion injury. <p><a href="https://greenmedinfo.com/article/advances-protective-effects-ginsenosides-myocardial-ischemia-and-ischemia-repe" target="_blank">read more</a></p> https://greenmedinfo.com/article/advances-protective-effects-ginsenosides-myocardial-ischemia-and-ischemia-repe#comments Ginsenosides Myocardial Ischemia Cardioprotective In Vitro Study Sat, 05 Sep 2020 22:46:05 +0000 greenmedinfo 226447 at https://greenmedinfo.com "A Palaeolithic diet improves glucose tolerance more than a Mediterranean-like diet in individuals with ischaemic heart disease." https://greenmedinfo.com/article/palaeolithic-diet-improves-glucose-tolerance-more-mediterranean-diet-individua PMID:  Diabetologia. 2007 Sep ;50(9):1795-807. Epub 2007 Jun 22. PMID: 17583796 Abstract Title:  A Palaeolithic diet improves glucose tolerance more than a Mediterranean-like diet in individuals with ischaemic heart disease. Abstract:  AIMS/HYPOTHESIS: Most studies of diet in glucose intolerance and type 2 diabetes have focused on intakes of fat, carbohydrate, fibre, fruits and vegetables. Instead, we aimed to compare diets that were available during human evolution with more recently introduced ones.METHODS: Twenty-nine patients with ischaemic heart disease plus either glucose intolerance or type 2 diabetes were randomised to receive (1) a Palaeolithic (&#039;Old Stone Age&#039;) diet (n = 14), based on lean meat, fish, fruits, vegetables, root vegetables, eggs and nuts; or (2) a Consensus (Mediterranean-like) diet (n = 15), based on whole grains, low-fat dairy products, vegetables, fruits, fish, oils and margarines. Primary outcome variables were changes in weight, waist circumference and plasma glucose AUC (AUC Glucose(0-120)) and plasma insulin AUC (AUC Insulin(0-120)) in OGTTs.RESULTS: Over 12 weeks, there was a 26% decrease of AUC Glucose(0-120) (p = 0.0001) in the Palaeolithic group and a 7% decrease (p = 0.08) in the Consensus group. The larger (p = 0.001) improvement in the Palaeolithic group was independent (p = 0.0008) of change in waist circumference (-5.6 cm in the Palaeolithic group, -2.9 cm in the Consensus group; p = 0.03). In the study population as a whole, there was no relationship between change in AUC Glucose(0-120) and changes in weight (r = -0.06, p = 0.9) or waist circumference (r = 0.01, p = 1.0). There was a tendency for a larger decrease of AUC Insulin(0-120) in the Palaeolithic group, but because of the strong association between change in AUC Insulin(0-120) and change in waist circumference (r = 0.64, p = 0.0003), this did not remain after multivariate analysis.CONCLUSIONS/INTERPRETATION: A Palaeolithic diet may improve glucose tolerance independently of decreased waist circumference. https://greenmedinfo.com/article/palaeolithic-diet-improves-glucose-tolerance-more-mediterranean-diet-individua#comments Diabetes Mellitus: Type 2 Heart Disease: Ischemic Myocardial Ischemia Dietary Modification: Paleolithic/Stone Age Diet Insulin Human Study Fri, 27 Jan 2012 19:51:51 +0000 greenmedinfo 70936 at https://greenmedinfo.com "Apoptosis inhibition of capsaicin on myocardial ischemia-reperfusion injury in rats" https://greenmedinfo.com/article/apoptosis-inhibition-capsaicin-myocardial-ischemia-reperfusion-injury-rats PMID:  Sichuan Da Xue Xue Bao Yi Xue Ban. 2011 Mar ;42(2):218-21. PMID: 21500557 Abstract Title:  [Apoptosis inhibition of capsaicin on myocardial ischemia-reperfusion injury in rats]. Abstract:  OBJECTIVE: To determine apoptosis inhibition effect of capsaicin on myocardial ischemia-reperfusion injury in rats and its underlying mechanisms.METHODS: The rat model of myocardial ischemia-reperfusion injury was established by ligating the left anterior descending coronary artery for 45 min and then loosing the ligation (reperfusion) for 120 min. Twenty healthy male rats were randomly divided into sham group, control group (I/R), capsaicin group (CAP+I/R), capsazepine group (CAPZ+CAP+I/R), and S-3144 group (S-3144+CAP+I/R). All drugs were delivered bolusly into left ventricle (LV)via right carotid artery at 10 min and 5 min before ischemia. Rats in I/R group and sham group only received vehicle injection. Myocardial protection was assessed by measurements of heart rate (HR) and left ventricular developed pressure (LVDP). The pathologic changes of myocardial tissue in each group were observed under light microscopy. TUNEL-positive nuclei were tested by immunofluorescent method.RESULTS: At 120 min after reperfusion, there were significant increases of HR and LVDP in CAP+I/R group when compared with control group, capsazepine group, and S-3144 group (P https://greenmedinfo.com/article/apoptosis-inhibition-capsaicin-myocardial-ischemia-reperfusion-injury-rats#comments Capsaicin Myocardial Infarction Myocardial Ischemia Anti-Apoptotic Cardioprotective Animal Study Wed, 19 Dec 2012 22:33:08 +0000 greenmedinfo 87306 at https://greenmedinfo.com 18β-glycyrrhetinic acid improves cardiac diastolic function by attenuating intracellular calcium overload. https://greenmedinfo.com/article/18-glycyrrhetinic-acid-improves-cardiac-diastolic-function-attenuating-intrace PMID:  Curr Med Sci. 2020 Aug ;40(4):654-661. Epub 2020 Aug 29. PMID: 32862375 Abstract Title:  18β-Glycyrrhetinic Acid Improves Cardiac Diastolic Function by Attenuating Intracellular Calcium Overload. Abstract:  Ranolazine, a late sodium current inhibitor, has been demonstrated to be effective on heart failure. 18β-glycyrrhetinic acid (18β-GA) has the similar inhibitory effect on late sodium currents. However, its effect on diastolic function is still unknown. This study aimed to determine whether 18β-GA can improve the diastolic function and to explore the underlying mechanisms. Eighty male Sprague Dawley (SD) rats of Langendorff model were randomly divided into the following groups: group A, normal cardiac perfusion group; group B, ischemia-reperfusion group; group C, ischemia-reperfusion with anemoniasulcata toxin II (ATX-II); group D, ranolazine group; and group E, 18β-GA group with four different concentrations. Furthermore, a pressure-overloaded rat model induced by trans-aortic constriction (TAC) was established. Echocardiography and hemodynamics were used to evaluate diastolic function at 14th day after TAC. Changes of free intracellular calcium (Ca) concentration was indirectly detected by laser scanning confocal microscope to confirm the inhibition of late sodium currents. With the intervention of ATX-II on ischemia reperfusion injury group, 5µmol/L ranolazine, and 5, 10, 20, 40 µmol/L 18β-GA could improve ATX-II-induced cardiac diastolic dysfunction. 630 mg/kg glycyrrhizin tablets could improve cardiac diastolic function in the pressure-overloaded rats. 18β-GA and ranolazine had similar effects on reducing the free calcium in cardiomyocytes. The study demonstrates that 18β-GA and glycyrrhizin could improve diastolic dysfunction induced by ischemia-reperfusion injury in Langendorff-perfused rat hearts and pressure-overloaded rats. The mechanism may be attributed to the inhibition of enhanced late sodium currents. <p><a href="https://greenmedinfo.com/article/18-glycyrrhetinic-acid-improves-cardiac-diastolic-function-attenuating-intrace" target="_blank">read more</a></p> https://greenmedinfo.com/article/18-glycyrrhetinic-acid-improves-cardiac-diastolic-function-attenuating-intrace#comments 18β-Glycyrrhetinic Acid Heart Failure Myocardial Ischemia Cardioprotective Animal Study Mon, 12 Oct 2020 16:02:34 +0000 greenmedinfo 228003 at https://greenmedinfo.com 2,3,5,4'-Tetrahydroxystilbene-2-O-β-D-glucoside protects murine hearts against ischemia/reperfusion injury. https://greenmedinfo.com/article/2354-tetrahydroxystilbene-2-o-d-glucoside-protects-murine-hearts-against-ische PMID:  Acta Pharmacol Sin. 2017 Mar ;38(3):317-330. Epub 2017 Jan 23. PMID: 28112174 Abstract Title:  2,3,5,4&#039;-Tetrahydroxystilbene-2-O-β-D-glucoside protects murine hearts against ischemia/reperfusion injury by activating Notch1/Hes1 signaling and attenuating endoplasmic reticulum stress. Abstract:  2,3,5,4&#039;-Tetrahydroxystilbene-2-O-β-D-glucoside (TSG) is a water-soluble active component extracted from Polygonum multiflorum Thunb. A number of studies demonstrate that TSG exerts cardioprotective effects. Since endoplasmic reticulum (ER) stress plays a key role in myocardial ischemia/reperfusion (MI/R)-induced cell apoptosis, wesought to determine whether modulation of the ER stress during MI/R injury was involved in the cardioprotective action of TSG. Male mice were treated with TSG (60 mg·kg·d, ig) for 2 weeks and then were subjected to MI/R surgery. Pre-administration of TSG significantly improved post-operative cardiac function, and suppressed MI/R-induced myocardial apoptosis, evidenced by the reduction in the myocardial apoptotic index, serum levels of LDH and CK after 6 h of reperfusion. TSG (0.1-1000μmol/L) did not affect the viability of cultured H9c2 cardiomyoblasts in vitro, but pretreatment with TSG dose-dependently decreased simulated ischemia/reperfusion (SIR)-induced cell apoptosis. Furthermore, both in vivo and in vitro studies revealed that TSG treatment activated the Notch1/Hes1 signaling pathway and suppressed ER stress, as evidenced by increasing Notch1, Notch1 intracellular domain (NICD), Hes1, and Bcl-2 expression levels and by decreasing p-PERK/PERK ratio, p-eIF2α/eIF2α ratio, and ATF4, CHOP, Bax, and caspase-3 expression levels. Moreover, the protective effects conferred by TSG on SIR-treated H9c2 cardiomyoblasts were abolished by co-administration of DAPT (the Notch1 signaling inhibitor). In summary, TSG ameliorates MI/R injury in vivo and in vitro by activating the Notch1/Hes1 signaling pathway and attenuating ER stress-induced apoptosis. <p><a href="https://greenmedinfo.com/article/2354-tetrahydroxystilbene-2-o-d-glucoside-protects-murine-hearts-against-ische" target="_blank">read more</a></p> https://greenmedinfo.com/article/2354-tetrahydroxystilbene-2-o-d-glucoside-protects-murine-hearts-against-ische#comments Myocardial Ischemia Anti-Apoptotic Cardioprotective Animal Study In Vitro Study Tue, 15 Jan 2019 01:28:59 +0000 greenmedinfo 177549 at https://greenmedinfo.com 6-Gingerol attenuates ischemia-reperfusion-induced cell apoptosis in human AC16 cardiomyocytes. https://greenmedinfo.com/article/6-gingerol-attenuates-ischemia-reperfusion-induced-cell-apoptosis-human-ac16-c PMID:  Evid Based Complement Alternat Med. 2019 ;2019:8798653. Epub 2019 Feb 11. PMID: 30886640 Abstract Title:  6-Gingerol Attenuates Ischemia-Reperfusion-Induced Cell Apoptosis in Human AC16 Cardiomyocytes through HMGB2-JNK1/2-NF-B Pathway. Abstract:  Myocardial ischemia/reperfusion (I/R) injury is a key factor in deterioration of myocardial function. The c-Jun NH2-terminal kinase (JNK) activation and the transcription factor nuclear factor-kappaB (NF-B) nuclear translocation have been found in I/R injury. 6-Gingerol, an important bioactive ingredient of ginger, has been reported to have cardiovascular pharmacological effects. However, the molecular mechanism through which it is beneficial is unclear. In this work, I/R induced the increase in the apoptosis and reactive oxygen species level in AC16 cardiomyocytes. 6-Gingerol administration decreased cardiomyocyte apoptosis and improved oxidative stress indexes. 6-Gingerol administration also inhibited I/R-induced HMGB2 expression upregulation and JNK activation and reduced Cleaved Poly(ADP-ribose) polymerases (PARP) and Caspase-3 expression. HMGB2 treatment mimicked the effect of I/R-induced cell damage, which was reversed by 6-gingerol administration. On the other hand, transcriptional activity of NF-B was reduced in 6-gingerol treated cells. Thus, overall results indicated that 6-gingerol administration protected I/R-induced cardiomyocytes apoptosis via JNK/NF-B pathway in the regulation of HMGB2. This work supported the efficacy of 6-gingerol on cardiovascular disease and partially revealed its mechanism, which was helpful for understanding the therapeutic effects of this natural drug. <p><a href="https://greenmedinfo.com/article/6-gingerol-attenuates-ischemia-reperfusion-induced-cell-apoptosis-human-ac16-c" target="_blank">read more</a></p> https://greenmedinfo.com/article/6-gingerol-attenuates-ischemia-reperfusion-induced-cell-apoptosis-human-ac16-c#comments Gingerol Myocardial Ischemia Anti-Apoptotic Cardioprotective Human In Vitro Fri, 05 Apr 2019 16:23:44 +0000 greenmedinfo 184303 at https://greenmedinfo.com 6-gingerol inhibits apoptosis to attenuate myocardial ischemia/reperfusion injury. https://greenmedinfo.com/article/6-gingerol-inhibits-apoptosis-attenuate-myocardial-ischemiareperfusion-injury PMID:  Evid Based Complement Alternat Med. 2018 ;2018:9024034. Epub 2018 Mar 20. PMID: 29743926 Abstract Title:  6-Gingerol Activates PI3K/Akt and Inhibits Apoptosis to Attenuate Myocardial Ischemia/Reperfusion Injury. Abstract:  6-Gingerol (6-G) is known to alleviate myocardial ischemia/reperfusion injury. However, the underlying molecular mechanisms of 6-G myocardial protection are not known. In this study, the protective effect of 6-G on ischemia/reperfusion (I/R) damage and whether such a mechanism was related to apoptosis inhibition and activation of phosphoinositide 3-kinases (PI3K)/serine/threonine kinase (Akt) signaling pathway were investigated. Rats were subjected to I/R in the presence or absence of 6-G and the changes of cardiac function, infarct size and histopathological changes, and the levels of cardiac troponin T, creatine kinase-MB, and myocardial apoptosis were examined. The expression of caspase-3, PI3K, p-Akt, and Akt was also determined. We found that 6-G (6 mg/kg) pretreatment significantly improved heart function and ameliorated infarct size and histopathological changes and cardiac troponin T and creatine kinase-MB levels induced by I/R. Moreover, pretreatment with 6-G significantly inhibited myocardial apoptosis and caspase-3 activation induced by I/R. 6-G also upregulated expression of PI3K, p-Akt, and Akt in myocardial tissues. Taken together, these findings suggest that 6-G inhibits apoptosis and activates PI3K/Akt signaling in response to myocardial I/R injury as a possible mechanism to attenuate I/R-induced injury in heart. These results might be important for developing novel strategies for preventing myocardial I/R injury. <p><a href="https://greenmedinfo.com/article/6-gingerol-inhibits-apoptosis-attenuate-myocardial-ischemiareperfusion-injury" target="_blank">read more</a></p> https://greenmedinfo.com/article/6-gingerol-inhibits-apoptosis-attenuate-myocardial-ischemiareperfusion-injury#comments Gingerol Myocardial Ischemia Anti-Apoptotic Cardioprotective Animal Study Sat, 21 Jul 2018 02:48:45 +0000 greenmedinfo 167736 at https://greenmedinfo.com 6-gingerol protects heart by suppressing myocardial ischemia/reperfusion induced inflammation. https://greenmedinfo.com/article/6-gingerol-protects-heart-suppressing-myocardial-ischemiareperfusion-induced-i PMID:  Evid Based Complement Alternat Med. 2018 ;2018:6209679. Epub 2018 Nov 5. PMID: 30519268 Abstract Title:  6-Gingerol Protects Heart by Suppressing Myocardial Ischemia/Reperfusion Induced Inflammation via the PI3K/Akt-Dependent Mechanism in Rats. Abstract:  Our previous study has demonstrated that 6-Gingerol (6-G) could alleviate myocardial ischemia/reperfusion injury (MIRI). However, the molecular mechanism underlying the process of myocardial ischemia/reperfusion (I/R) injury alleviation by 6-G remains unelucidated. The objective of the present study is to further investigate the potential mechanism for 6-G to alleviate MIRI in rats. Thirty-two Sprague-Dawley rats were randomly divided into four groups: the Sham group, the I/R group, the 6-G + I/R group, and the LY294002 (LY) + 6-G + I/R group. For the rats in each of the groups, data were collected for cardiogram, cardiac function, area of myocardial infarction, myocardial pathology, myocardial enzyme, marker of inflammatory response, and PI3K/Akt signaling pathway. We found that the pretreatment of 6-G with 6 mg/kg could shrink the ST section of cardiogram, improve the cardiac function, reduce the area of myocardial infarction and the degree of cardiac pathological injury, lower the level of myocardial enzyme, and inhibit the inflammatory response. In addition, our results also indicated that 6-G could upregulate the expression of PI3K and p-Akt and that LY294002, a blocking agent of PI3K/Akt signaling pathway, could nullify the protecting role of 6-G. Our experimental results showed that 6-G could inhibit I/R-induced inflammatory response through the activation of the PI3K/Akt signaling pathway. <p><a href="https://greenmedinfo.com/article/6-gingerol-protects-heart-suppressing-myocardial-ischemiareperfusion-induced-i" target="_blank">read more</a></p> https://greenmedinfo.com/article/6-gingerol-protects-heart-suppressing-myocardial-ischemiareperfusion-induced-i#comments Gingerol Myocardial Ischemia Anti-Inflammatory Agents Cardioprotective Animal Study Tue, 18 Dec 2018 20:29:02 +0000 greenmedinfo 175992 at https://greenmedinfo.com 6-Gingerol relieves myocardial ischaemia/reperfusion injury. https://greenmedinfo.com/article/6-gingerol-relieves-myocardial-ischaemiareperfusion-injury PMID:  Lab Invest. 2021 Mar 23. Epub 2021 Mar 23. PMID: 33758383 Abstract Title:  6-Gingerol relieves myocardial ischaemia/reperfusion injury by regulating lncRNA H19/miR-143/ATG7 signaling axis-mediated autophagy. Abstract:  Myocardial ischemia/reperfusion injury (MIRI) causes severe damage in cardiac tissue, thereby resulting in a high rate of mortality. 6-Gingerol (6-G) is reported to play an essential role in alleviating MIRI. However, the underlying mechanism remains obscure. This study was intended to explore the potential mechanism by which 6-G functions. Q-PCR was employed to quantify the relative RNA levels of long noncoding RNA (lncRNA) H19 (H19), miR-143, and ATG7, an enzyme essential for autophagy, in HL-1 cells. Western blotting, immunofluorescence, and immunohistochemistry were employed for protein evaluation in cultured cells or mouse tissues. Cell viability, cytotoxicity, and apoptosis were analysed by CCK-8, LDH, and flow cytometry assays, respectively. The binding sites for miR-143 were predicted using starBase software and experimentally validated through a dual-luciferase reporter system. Here, we found that 6-G elevated cellular H19 expression in hypoxia/reoxygenation (H/R)-treated HL-1 cells. Moreover, 6-G increased Bcl-2 expression but reduced cleaved caspase 3 and caspase 9 protein levels. Mechanistically, H19 directly interacted with miR-143 and lowered its cellular abundance by acting as a molecular sponge. Importantly, ATG7 was validated as a regulated gene of miR-143, and the depletion of miR-143 by H19 caused an increased in ATG7 expression, which in turn promoted the autophagy process. Last, mouse experiments highly supported our in vitro findings that 6-G relieves MIRI by enhancing autophagy. The H19/miR-143/ATG7 axis was shown to be critical for the function of 6-G in relieving MIRI. <p><a href="https://greenmedinfo.com/article/6-gingerol-relieves-myocardial-ischaemiareperfusion-injury" target="_blank">read more</a></p> https://greenmedinfo.com/article/6-gingerol-relieves-myocardial-ischaemiareperfusion-injury#comments Gingerol Myocardial Ischemia Anti-Apoptotic Cardioprotective MicroRNA modulator Animal Study Sat, 08 May 2021 03:10:49 +0000 greenmedinfo 239308 at https://greenmedinfo.com 6-shogaol from dried ginger protects against intestinal ischemia/reperfusion. https://greenmedinfo.com/article/6-shogaol-dried-ginger-protects-against-intestinal-ischemiareperfusion PMID:  Mol Nutr Food Res. 2023 Jul ;67(13):e2200773. Epub 2023 May 14. PMID: 37118920 Abstract Title:  6-Shogaol from Dried Ginger Protects against Intestinal Ischemia/Reperfusion by Inhibiting Cell Apoptosis via the BDNF/TrkB/PI3K/AKT Pathway. Abstract:  SCOPE: Intestinal ischemia-reperfusion (II/R) injury is a common pathological process with high morbidity and mortality. Effective prevention and treatment therapies for II/R are clinically necessary. 6-Shogaol (6-SG), the main active ingredient in dried ginger, behaviors multiple biological activities, including anti-inflammation, antioxidation, and anti-apoptosis. This study aims to elucidate the protective effects and mechanism of 6-SG against II/R-induced injury.METHODS AND RESULTS: Sprague-Dawley rats are pre-treated orally with 6-SG and subjected to II/R injury by clamping superior mesenteric artery for 1 h and reperfusion for 2 h. Caco-2 cells are challenged by hypoxia/reoxygenation to mimic II/R in vitro. 6-SG pre-treatment protects against II/R injury by reducing intestinal morphological damage and intestinal barrier injury via inhibiting cell apoptosis. Network pharmacology and molecular docking analyses reveal that 6-SG has a high affinity with brain-derived neurotrophic factor (BDNF) formed homodimer or heterodimer with NT4 instead of the monomer, and thus the dimer configuration is stabilized, activating BDNF/TrkB/PI3K/AKT signaling pathway and inhibiting II/R-induced cell apoptosis. The outcome is further validated both in vivo and in vitro.CONCLUSION: 6-Shogaol protects against II/R injury by inhibiting cell apoptosis through the BDNF/TrkB/PI3K/AKT pathway. This study offers a new understanding of the protection mechanism of 6-SG against II/R-induced injury. <p><a href="https://greenmedinfo.com/article/6-shogaol-dried-ginger-protects-against-intestinal-ischemiareperfusion" target="_blank">read more</a></p> https://greenmedinfo.com/article/6-shogaol-dried-ginger-protects-against-intestinal-ischemiareperfusion#comments 6-Shogaol Ginger Myocardial Ischemia Anti-Apoptotic Cardioprotective Animal Study Sun, 30 Jul 2023 18:28:25 +0000 greenmedinfo 277262 at https://greenmedinfo.com A combination of ω-3 PUFA and AA treatment confers an additive effect in suppressing lipid peroxidation and improving myocardial function. https://greenmedinfo.com/article/combination-3-pufa-and-aa-treatment-confers-additive-effect-suppressing-lipid- PMID:  Biomed Pharmacother. 2020 Nov 7 ;133:110970. Epub 2020 Nov 7. PMID: 33166763 Abstract Title:  Effects ofω-3 PUFA and ascorbic acid combination on post-resuscitation myocardial function. Abstract:  Accumulating evidence demonstrated that administration ofω-3 polyunsaturated fatty acid (ω-3 PUFA) or ascorbic acid (AA) following cardiac arrest (CA) improves survival. Therefore, we investigate the effects of ω-3 PUFA combined with AA on myocardial function after CA and cardiopulmonary resuscitation (CPR) in a rat model. Thirty male rats were randomized into 5 groups: (1) sham; (2) control; (3) ω-3 PUFA; (4) AA; (5) ω-3 PUFA + AA. Ventricular fibrillation (VF) was induced and untreated for 6 min followed by defibrillation after 8 min of CPR. Infusion of drug or vehicle occurred at the start of CPR. Myocardial function and sublingual microcirculation were measured at baseline and after return of spontaneous circulation (ROSC). Heart tissues and blood were collected 6 h after ROSC. Myocardial function and sublingual microcirculation improvements were seen with ω-3 PUFA or AA compared to control after ROSC (p<p><a href="https://greenmedinfo.com/article/combination-3-pufa-and-aa-treatment-confers-additive-effect-suppressing-lipid-" target="_blank">read more</a></p> https://greenmedinfo.com/article/combination-3-pufa-and-aa-treatment-confers-additive-effect-suppressing-lipid-#comments Myocardial Ischemia Omega-3 Fatty Acids Vitamin C Antioxidants Cardioprotective Animal Study Sat, 14 Nov 2020 18:53:16 +0000 greenmedinfo 229632 at https://greenmedinfo.com A functional polysaccharide from Eriobotrya japonica relieves myocardial ischemia injury. https://greenmedinfo.com/article/functional-polysaccharide-eriobotrya-japonica-relieves-myocardial-ischemia-inj PMID:  Food Funct. 2022 Jan 4 ;13(1):113-120. Epub 2022 Jan 4. PMID: 34878451 Abstract Title:  A functional polysaccharide fromrelieves myocardial ischemia injuryanti-oxidative and anti-inflammatory effects. Abstract:  We herein report a food-derived polysaccharide (EJP) with the effect of relieving myocardial ischemia reperfusion injury (MIRI). This novel polysaccharide was isolated from the leaf of, and we first found its myocardium protective effects. Then, we firstly characterized EJP with a series of analytical technologies and further tested its effect on myocardial ischemia reperfusion injury (MIRI) with the illustration of the potential mechanisms. Interestingly, in the murine model of MIRI, administration of EJP effectively improved post-I/R heart contraction and limited the infarct size. Moreover, EJP significantly attenuated IR-induced oxidative damage and inflammatory reaction, as evidenced by decreasing MDA, IL-6, and TNF-α contents and increasing SOD activity and GSH-Px expression. In addition, we proved that EJP not only had no nephrotoxicity but also demonstrated a protective effect on the kidneys through HE staining and biochemical analysis. In sum, EJP, with a significant protective effect against myocardial I/R injury by showing anti-inflammatory and anti-oxidative activities, may become a meaningful drug candidate for the treatment of myocardial I/R injury. <p><a href="https://greenmedinfo.com/article/functional-polysaccharide-eriobotrya-japonica-relieves-myocardial-ischemia-inj" target="_blank">read more</a></p> https://greenmedinfo.com/article/functional-polysaccharide-eriobotrya-japonica-relieves-myocardial-ischemia-inj#comments Loquat Myocardial Ischemia Anti-Inflammatory Agents Antioxidants Cardioprotective Interleukin-6 Downregulation Malondialdehyde Down-regulation Tumor Necrosis Factor (TNF) Alpha Inhibitor Animal Study Mon, 12 Sep 2022 00:17:06 +0000 greenmedinfo 263286 at https://greenmedinfo.com