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1.
Transplant Proc ; 51(8): 2823-2827, 2019 Oct.
Article in English | MEDLINE | ID: mdl-31493918

ABSTRACT

OBJECTIVE: Hepatic ischemia reperfusion (I/R) injury is regarded as a serious concern in clinical practice. Citric acid reduces oxidative stress and inflammation during hypoxia and reoxygenation. Our objective was to investigate the protective effect of citric acid against hepatic I/R injury in rats. METHODS: We fed Sprague-Dawley rats either citric acid (100 mg/kg/d) or saline. One week later, ischemia was induced by clamping the rats' common hepatic artery and portal vein for 30 minutes. The rats were randomly divided into 3 major groups that were treated as follows: 1. the sham operated group; 2. the I/R group; and 3. the I/R-citric acid group. RESULTS: Compared to the sham group, the I/R group had higher expression of aspartate aminotransferase and alanine aminotransferase and lower expression of catalase, superoxide dismutase, glutathione peroxidase, antioxidant, nitric oxide, and albumin. Compared to the I/R group, the I/R-citric acid group had higher expression of catalase, superoxide dismutase, antioxidants, and nitric oxide, and lower expression of aspartate aminotransferase and alanine aminotransferase. CONCLUSIONS: These results suggest that citric acid therapy has significant therapeutic potential in ischemic liver injury.


Subject(s)
Antioxidants/therapeutic use , Citric Acid/therapeutic use , Liver Diseases/prevention & control , Liver/blood supply , Reperfusion Injury/prevention & control , Alanine Transaminase/metabolism , Animals , Antioxidants/pharmacology , Aspartate Aminotransferases/metabolism , Catalase/metabolism , Citric Acid/pharmacology , Glutathione Peroxidase/metabolism , Liver Diseases/metabolism , Male , Nitric Oxide/metabolism , Oxidative Stress/drug effects , Rats , Rats, Sprague-Dawley , Reperfusion Injury/metabolism , Superoxide Dismutase/metabolism
2.
Transplant Proc ; 51(8): 2838-2841, 2019 Oct.
Article in English | MEDLINE | ID: mdl-31493919

ABSTRACT

OBJECTIVE: Hesperidin is a well-known flavanone glycoside copiously found in sweet orange and lemon, which was recently reported to possess significant anti-inflammatory, analgesic, antifungal, antiviral, antioxidant, and anticancer activities. Ischemia-reperfusion (I/R) injury is a major problem after renal transplantation. Furthermore, inflammatory responses to I/R exacerbate the resultant renal injury. In the present study, we investigated whether hesperidin exhibits renoprotective effects against I/R-induced acute kidney injury in a rat model. METHODS: We fed Sprague-Dawley rats either hesperidin (100 mg/kg/d) or saline. One week later, ischemia was induced by bilateral renal pedicle occlusion for 30 minutes followed by reperfusion. The rats were randomly divided into 3 groups, which were treated as follows: 1. the sham operated group; 2. the I/R group; 3. the I/R-hesperidin group RESULTS: Compared to the sham group, the I/R group had higher expression of blood urea nitrogen and serum creatinine and lower expression of catalase, superoxide dismutase, glutathione peroxidase, antioxidants, and nitric oxide. Compared to the I/R group, the I/R-hesperidin group had higher expression of catalase, superoxide dismutase, glutathione peroxidase, antioxidant, and nitric oxide and lower expression of blood urea nitrogen and serum creatinine. CONCLUSIONS: Hesperidin improved acute renal I/R injury through its antioxidant effects. These findings suggest that hesperidin is a potential therapeutic agent for acute ischemia-induced renal damage.


Subject(s)
Acute Kidney Injury/prevention & control , Antioxidants/therapeutic use , Hesperidin/therapeutic use , Kidney/blood supply , Reperfusion Injury/prevention & control , Acute Kidney Injury/metabolism , Animals , Antioxidants/pharmacology , Blood Urea Nitrogen , Catalase/metabolism , Creatinine/blood , Glutathione Peroxidase/metabolism , Hesperidin/pharmacology , Kidney/drug effects , Male , Nitric Oxide/metabolism , Rats , Rats, Sprague-Dawley , Reperfusion Injury/metabolism , Superoxide Dismutase/metabolism
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