We are analyzing https://link.springer.com/article/10.1007/s12291-019-00848-7.

Title:
The Nephroprotective Effect of Lycopene on Renal Ischemic Reperfusion Injury: A Mouse Model | Indian Journal of Clinical Biochemistry
Description:
Acute kidney injury (AKI) is characterized by fast decline in renal function within a short period of time. Renal ischemic–reperfusion (I–R) injury is the main cause of AKI. This study aims to investigate the possible nephroprotective effect of lycopene on renal ischemic–reperfusion injury in mice model. Forty Swiss Albino adult male mice were randomly allocated onto one of the four study groups: sham group: mice had median laparotomy under anesthesia with no procedures performed, renal tissues and blood samples were collected. ischemic–reperfusion group (I–R-control): mice underwent median laparotomy under anesthesia, followed by 30 min bilateral renal ischemia. Renal tissues and blood samples were collected after 2 h from reperfusion. Vehicle-treated group: mice were pretreated with intra 1% dimethyl sulfoxide 30 min before inducing ischemia. Lycopene-treated group: mice were pretreated with 10 mg/kg intraperitoneal injection of lycopene 30 min before inducing renal ischemia. Renal tissues, and blood samples were collected after 2 h from reperfusion. Blood and tissue samples were collected to look for evidence of inflammation and necrosis. Blood urea nitrogen, serum creatinine as well as plasma NGAL levels were significantly increased in the active control group (P ≤ 0.05), when compared to the sham group. Similarly, renal levels of Notch2/Hes 1, TLR 2, IL-6, Bax, and F2-isoprostane were significantly increased in the active control group as compared to the sham group (P ≤ 0.05). Moreover, lycopene treatment was found to be significantly effective in reducing the increased levels of these markers after I–R injury (P ≤ 0.05).
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Topics {✒️}

nf-κb signaling pathway tlr/nf-kappab pathway renal ischemia/reperfusion injury renal ischemia-reperfusion injury acute renal ischaemia/reperfusion renal ischemic–reperfusion injury acute kidney injury month download article/chapter high-throughput flow cytometry d-optimal mixture design 10 mg/kg intraperitoneal injection tomato-based sauce formulations renal ischemic–reperfusion ischemia-reperfusion model inducing renal ischemia accelerated kidney ageing article indian journal oxidative stress fas/fasl pathway post injury fibrosis chronic kidney disease full article pdf ischemic–reperfusion group privacy choices/manage cookies notch2/hes 1 physiol renal physiol valproic acid nat rev nephrol traditional indian plants jamil da lycopene isomer profile exp cell res clin exp nephrol european economic area ketamine-xylazine preparations de caestecker mp visual exp jove daily peritoneal administration dialysis solution prevents acta cirurgica brasileira de kretser dm cell-based screening conditions privacy policy 2023 anti-inflammatory effects early disease detection vehicle-treated group kidney podocytes lycopene-treated group clinical biochemistry aims oliva trejo ja

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         headline:The Nephroprotective Effect of Lycopene on Renal Ischemic Reperfusion Injury: A Mouse Model
         description:Acute kidney injury (AKI) is characterized by fast decline in renal function within a short period of time. Renal ischemic–reperfusion (I–R) injury is the main cause of AKI. This study aims to investigate the possible nephroprotective effect of lycopene on renal ischemic–reperfusion injury in mice model. Forty Swiss Albino adult male mice were randomly allocated onto one of the four study groups: sham group: mice had median laparotomy under anesthesia with no procedures performed, renal tissues and blood samples were collected. ischemic–reperfusion group (I–R-control): mice underwent median laparotomy under anesthesia, followed by 30 min bilateral renal ischemia. Renal tissues and blood samples were collected after 2 h from reperfusion. Vehicle-treated group: mice were pretreated with intra 1% dimethyl sulfoxide 30 min before inducing ischemia. Lycopene-treated group: mice were pretreated with 10 mg/kg intraperitoneal injection of lycopene 30 min before inducing renal ischemia. Renal tissues, and blood samples were collected after 2 h from reperfusion. Blood and tissue samples were collected to look for evidence of inflammation and necrosis. Blood urea nitrogen, serum creatinine as well as plasma NGAL levels were significantly increased in the active control group (P ≤ 0.05), when compared to the sham group. Similarly, renal levels of Notch2/Hes 1, TLR 2, IL-6, Bax, and F2-isoprostane were significantly increased in the active control group as compared to the sham group (P ≤ 0.05). Moreover, lycopene treatment was found to be significantly effective in reducing the increased levels of these markers after I–R injury (P ≤ 0.05).
         datePublished:2019-09-13T00:00:00Z
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      headline:The Nephroprotective Effect of Lycopene on Renal Ischemic Reperfusion Injury: A Mouse Model
      description:Acute kidney injury (AKI) is characterized by fast decline in renal function within a short period of time. Renal ischemic–reperfusion (I–R) injury is the main cause of AKI. This study aims to investigate the possible nephroprotective effect of lycopene on renal ischemic–reperfusion injury in mice model. Forty Swiss Albino adult male mice were randomly allocated onto one of the four study groups: sham group: mice had median laparotomy under anesthesia with no procedures performed, renal tissues and blood samples were collected. ischemic–reperfusion group (I–R-control): mice underwent median laparotomy under anesthesia, followed by 30 min bilateral renal ischemia. Renal tissues and blood samples were collected after 2 h from reperfusion. Vehicle-treated group: mice were pretreated with intra 1% dimethyl sulfoxide 30 min before inducing ischemia. Lycopene-treated group: mice were pretreated with 10 mg/kg intraperitoneal injection of lycopene 30 min before inducing renal ischemia. Renal tissues, and blood samples were collected after 2 h from reperfusion. Blood and tissue samples were collected to look for evidence of inflammation and necrosis. Blood urea nitrogen, serum creatinine as well as plasma NGAL levels were significantly increased in the active control group (P ≤ 0.05), when compared to the sham group. Similarly, renal levels of Notch2/Hes 1, TLR 2, IL-6, Bax, and F2-isoprostane were significantly increased in the active control group as compared to the sham group (P ≤ 0.05). Moreover, lycopene treatment was found to be significantly effective in reducing the increased levels of these markers after I–R injury (P ≤ 0.05).
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         Pathology
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