Cardioprotective effect of Rosa canina L. methanolic extract on heat shock induced cardiomyocyte injury: An experimental study
Introduction: Overexposure to heat conditions can affect the functioning of the cardiovascular system and may promote cardiovascular disorders. Heat shock induced myocardial injury via increasing endoplasmic reticulum response-mediated apoptosis. This study investigated the impact of pretreatment wi...
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| Format: | Article |
| Language: | English |
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Tabriz University of Medical Sciences
2020-12-01
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| Series: | Journal of Cardiovascular and Thoracic Research |
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| Online Access: | https://jcvtr.tbzmed.ac.ir/PDF/jcvtr-12-286.pdf |
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| author | Ava Nasrolahi Leila Hosseini Fatemeh Farokhi-Sisakht Javad Mahmoudi Pouran Karimi Reza Badalzadeh Marjan Erfani |
| author_facet | Ava Nasrolahi Leila Hosseini Fatemeh Farokhi-Sisakht Javad Mahmoudi Pouran Karimi Reza Badalzadeh Marjan Erfani |
| author_sort | Ava Nasrolahi |
| collection | DOAJ |
| description | Introduction: Overexposure to heat conditions can affect the functioning of the cardiovascular system and may promote cardiovascular disorders. Heat shock induced myocardial injury via increasing endoplasmic reticulum response-mediated apoptosis. This study investigated the impact of pretreatment with Rosa canina (RC), a natural antioxidant, on myocardial damage induced by heat stress exposure and underlying mechanisms in cardiomyocytes in rats. Methods: Sixty adult male Wistar rats were allocated into five groups, including Control: received normal saline (NS), Heat Stress (HS), and HS+RC groups. Animals in the HS groups were subjected to heat stress (43 ºC) for 15 minutes once a day for two weeks. Animals in the HS+RC groups received three doses of RC (250, 500, and 1000 mg/mL) one hour before being subjected to heat shock. The endoplasmic reticulum (ER) transmembrane kinases, including PKR-like endoplasmic reticulum kinase (PERK), immunoreactivity of CCAAT/enhancer-binding protein homologous protein (CHOP), and eukaryotic translation initiation factor 2-alpha (eIF2α) as well as caspase 8 were detected by Western blot. The levels of reactive oxygen species (ROS) were assessed. Moreover, histopathological changes and apoptosis were also assayed in the heart tissue by using histopathological and TUNEL assays. Results: Heat exposure increased the level of ROS and induced oxidative damage in the heart tissue. The results demonstrated that RC administration decreased the overproduction of ROS induced by heat stress in cardiomyocytes. Moreover, heat stress up regulated the expression of p-PERK, p-eIF2α,and CHOP protein while pretreatment with RC decreased expression of ER stress-related markers in cardiomyocytes. Besides, RC diminished heat stress-induced cellular damage and apoptosis associated with inhibition of caspase 8 activation, a pro-apoptotic protein in cardiomyocytes. Conclusion: These findings indicate that RC exerts a protective effect on heart tissue, at least in part,through inactivation of PERK/eIF2α/CHOP pathway or inhibition of ER stress and oxidative stress triggeredapoptosis in cardiomyocytes induced by heat stress. |
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| institution | Directory Open Access Journal |
| issn | 2008-5117 2008-6830 |
| language | English |
| last_indexed | 2024-12-17T03:32:30Z |
| publishDate | 2020-12-01 |
| publisher | Tabriz University of Medical Sciences |
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| series | Journal of Cardiovascular and Thoracic Research |
| spelling | doaj.art-db93e58411224eb79c19aa90715ba1132022-12-21T22:05:14ZengTabriz University of Medical SciencesJournal of Cardiovascular and Thoracic Research2008-51172008-68302020-12-0112428629310.34172/jcvtr.2020.47jcvtr-28898Cardioprotective effect of Rosa canina L. methanolic extract on heat shock induced cardiomyocyte injury: An experimental studyAva Nasrolahi0Leila Hosseini1Fatemeh Farokhi-Sisakht2Javad Mahmoudi3Pouran Karimi4Reza Badalzadeh5Marjan Erfani6Infectious Ophthalmologic Research Center, Health Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, IranNeurosciences Research Center (NSRC), Tabriz University of Medical Sciences, Tabriz, IranNeurosciences Research Center (NSRC), Tabriz University of Medical Sciences, Tabriz, IranNeurosciences Research Center (NSRC), Tabriz University of Medical Sciences, Tabriz, IranNeurosciences Research Center (NSRC), Tabriz University of Medical Sciences, Tabriz, IranDepartment of Physiology, Tabriz University of Medical Sciences, Tabriz, IranNeurosciences Research Center (NSRC), Tabriz University of Medical Sciences, Tabriz, IranIntroduction: Overexposure to heat conditions can affect the functioning of the cardiovascular system and may promote cardiovascular disorders. Heat shock induced myocardial injury via increasing endoplasmic reticulum response-mediated apoptosis. This study investigated the impact of pretreatment with Rosa canina (RC), a natural antioxidant, on myocardial damage induced by heat stress exposure and underlying mechanisms in cardiomyocytes in rats. Methods: Sixty adult male Wistar rats were allocated into five groups, including Control: received normal saline (NS), Heat Stress (HS), and HS+RC groups. Animals in the HS groups were subjected to heat stress (43 ºC) for 15 minutes once a day for two weeks. Animals in the HS+RC groups received three doses of RC (250, 500, and 1000 mg/mL) one hour before being subjected to heat shock. The endoplasmic reticulum (ER) transmembrane kinases, including PKR-like endoplasmic reticulum kinase (PERK), immunoreactivity of CCAAT/enhancer-binding protein homologous protein (CHOP), and eukaryotic translation initiation factor 2-alpha (eIF2α) as well as caspase 8 were detected by Western blot. The levels of reactive oxygen species (ROS) were assessed. Moreover, histopathological changes and apoptosis were also assayed in the heart tissue by using histopathological and TUNEL assays. Results: Heat exposure increased the level of ROS and induced oxidative damage in the heart tissue. The results demonstrated that RC administration decreased the overproduction of ROS induced by heat stress in cardiomyocytes. Moreover, heat stress up regulated the expression of p-PERK, p-eIF2α,and CHOP protein while pretreatment with RC decreased expression of ER stress-related markers in cardiomyocytes. Besides, RC diminished heat stress-induced cellular damage and apoptosis associated with inhibition of caspase 8 activation, a pro-apoptotic protein in cardiomyocytes. Conclusion: These findings indicate that RC exerts a protective effect on heart tissue, at least in part,through inactivation of PERK/eIF2α/CHOP pathway or inhibition of ER stress and oxidative stress triggeredapoptosis in cardiomyocytes induced by heat stress.https://jcvtr.tbzmed.ac.ir/PDF/jcvtr-12-286.pdfrosa caninaoxidative stressendoplasmic reticulum stressheat stresscell death |
| spellingShingle | Ava Nasrolahi Leila Hosseini Fatemeh Farokhi-Sisakht Javad Mahmoudi Pouran Karimi Reza Badalzadeh Marjan Erfani Cardioprotective effect of Rosa canina L. methanolic extract on heat shock induced cardiomyocyte injury: An experimental study Journal of Cardiovascular and Thoracic Research rosa canina oxidative stress endoplasmic reticulum stress heat stress cell death |
| title | Cardioprotective effect of Rosa canina L. methanolic extract on heat shock induced cardiomyocyte injury: An experimental study |
| title_full | Cardioprotective effect of Rosa canina L. methanolic extract on heat shock induced cardiomyocyte injury: An experimental study |
| title_fullStr | Cardioprotective effect of Rosa canina L. methanolic extract on heat shock induced cardiomyocyte injury: An experimental study |
| title_full_unstemmed | Cardioprotective effect of Rosa canina L. methanolic extract on heat shock induced cardiomyocyte injury: An experimental study |
| title_short | Cardioprotective effect of Rosa canina L. methanolic extract on heat shock induced cardiomyocyte injury: An experimental study |
| title_sort | cardioprotective effect of rosa canina l methanolic extract on heat shock induced cardiomyocyte injury an experimental study |
| topic | rosa canina oxidative stress endoplasmic reticulum stress heat stress cell death |
| url | https://jcvtr.tbzmed.ac.ir/PDF/jcvtr-12-286.pdf |
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