{"title":"蜂胶对LPS致肾损害的抗氧化作用","authors":"Z. Doğanyiğit, B. Yakan, A. Okan, S. Silici","doi":"10.2478/ebtj-2020-0018","DOIUrl":null,"url":null,"abstract":"Abstract Sepsis is a systemic infectious disease that leads to shock, organ failure, and death and requires urgent treatment. Animal model studies of sepsis and endotoxemia have revealed that antioxidant compounds prevent the progression of multi-system organ failure and reduce death rate. In the present study aimed to establish the effect of propolis, which has been proven to have antibacterial, anti-inflammatory and antioxidant activities in recent years, on lipopolysaccharide (LPS)-induced renal damage. 40 Sprague dawley rats were randomly divided into five equal groups (n = 8): Control (0.9% NaCl), LPS (30 mg/kg), propolis (250 mg/kg), propolis + LPS, and LPS + propolis. After completion of the experimental protocol, Malondialdehyde (MDA) levels were measured using blood serum samples obtained from the rats. The kidney samples of the rats were examined histopathologically. As a result, it was determined that LPS increased MDA levels in the blood serum samples and it caused histological changes in the kidney tissue such as tubular damage, mild ischemic injury, ischemic damage in the form of vacuolization, tubular epithelial vacuolization, vascular congestion, and glomerular atrophy. Contrary to these results, MDA levels of serum decreased in the propolis + LPS, and LPS + propolis groups, and also histological findings improved. These results showed that protective effect of propolis against kidney damage caused by LPS.","PeriodicalId":22379,"journal":{"name":"The EuroBiotech Journal","volume":null,"pages":null},"PeriodicalIF":1.2000,"publicationDate":"2020-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"2","resultStr":"{\"title\":\"Antioxidative role of propolis on LPS induced renal damage\",\"authors\":\"Z. Doğanyiğit, B. Yakan, A. Okan, S. Silici\",\"doi\":\"10.2478/ebtj-2020-0018\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Abstract Sepsis is a systemic infectious disease that leads to shock, organ failure, and death and requires urgent treatment. Animal model studies of sepsis and endotoxemia have revealed that antioxidant compounds prevent the progression of multi-system organ failure and reduce death rate. In the present study aimed to establish the effect of propolis, which has been proven to have antibacterial, anti-inflammatory and antioxidant activities in recent years, on lipopolysaccharide (LPS)-induced renal damage. 40 Sprague dawley rats were randomly divided into five equal groups (n = 8): Control (0.9% NaCl), LPS (30 mg/kg), propolis (250 mg/kg), propolis + LPS, and LPS + propolis. After completion of the experimental protocol, Malondialdehyde (MDA) levels were measured using blood serum samples obtained from the rats. The kidney samples of the rats were examined histopathologically. As a result, it was determined that LPS increased MDA levels in the blood serum samples and it caused histological changes in the kidney tissue such as tubular damage, mild ischemic injury, ischemic damage in the form of vacuolization, tubular epithelial vacuolization, vascular congestion, and glomerular atrophy. Contrary to these results, MDA levels of serum decreased in the propolis + LPS, and LPS + propolis groups, and also histological findings improved. These results showed that protective effect of propolis against kidney damage caused by LPS.\",\"PeriodicalId\":22379,\"journal\":{\"name\":\"The EuroBiotech Journal\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":1.2000,\"publicationDate\":\"2020-07-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"2\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"The EuroBiotech Journal\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.2478/ebtj-2020-0018\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"MULTIDISCIPLINARY SCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"The EuroBiotech Journal","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.2478/ebtj-2020-0018","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"MULTIDISCIPLINARY SCIENCES","Score":null,"Total":0}
Antioxidative role of propolis on LPS induced renal damage
Abstract Sepsis is a systemic infectious disease that leads to shock, organ failure, and death and requires urgent treatment. Animal model studies of sepsis and endotoxemia have revealed that antioxidant compounds prevent the progression of multi-system organ failure and reduce death rate. In the present study aimed to establish the effect of propolis, which has been proven to have antibacterial, anti-inflammatory and antioxidant activities in recent years, on lipopolysaccharide (LPS)-induced renal damage. 40 Sprague dawley rats were randomly divided into five equal groups (n = 8): Control (0.9% NaCl), LPS (30 mg/kg), propolis (250 mg/kg), propolis + LPS, and LPS + propolis. After completion of the experimental protocol, Malondialdehyde (MDA) levels were measured using blood serum samples obtained from the rats. The kidney samples of the rats were examined histopathologically. As a result, it was determined that LPS increased MDA levels in the blood serum samples and it caused histological changes in the kidney tissue such as tubular damage, mild ischemic injury, ischemic damage in the form of vacuolization, tubular epithelial vacuolization, vascular congestion, and glomerular atrophy. Contrary to these results, MDA levels of serum decreased in the propolis + LPS, and LPS + propolis groups, and also histological findings improved. These results showed that protective effect of propolis against kidney damage caused by LPS.