Abstract
Abstract Objective In this study, possible protective effects of protocatechuic acid (PCA) against experimentally-induced acute renal ischemia/reperfusion (I/R) damage in rats, on matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9) and the associated signal transduction pathways were investigated. Methods A total of 3–4 month-old, 200–250 g Sprague Dawley rats were divided into groups of five (n=7). A right kidney nephrectomy surgery was conducted to all groups under anesthesia. Rats were administered polyethylene glycol 1 h prior to ischemia (Group I, II) and PCA (Group III, IV, V) intraperitoneally. Forty five minutes before the ischemia during 24 h reperfusion on all rats except those in Group I. At the end of the experiment, blood urea nitrogen (BUN), creatinine values and superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) enzyme levels were investigated in blood serum. MMP-2 and MMP-9 gene expression levels were determined by RT-PCR, and p38 and p-p38 protein expression levels Western blotting method. Renal tissue was examined histologically and immunohistochemically. Results It is assumed that 80 and 120 mg/kg of PCA might have a protective effect against oxidative stress damage caused by renal I/R. Conclusion In our study, PCA has been shown to modulate the increased expression of MMP-2 and MMP-9 mRNA along with increased oxidative stress during renal I/R, as well as oxidative damage-induced p38 protein expression. It was determined that particularly 120 mg kg−1 PCA reduced the renal I/R injury at a rate of 35–45%.
Highlights
Ischemia/reperfusion (I/R) damage is one of the main causes of acute kidney damage, and can develop in conditions such as hemorrhagic shock, partial nephrectomy, kidney transplant, and urological surgical procedures, causing organ loss due to temporary interruption of blood flow to the kidneys [1, 2]
When Group II was compared with Group III, IV and V, no significant differences were detected at the blood urea nitrogen (BUN) levels of Group III and IV compared to Group II (p>0.05); a significant difference was detected in Group IV compared to Group II (p
Significant differences were detected at the creatinine levels of Group IV and V compared to Group II (p0.05)
Summary
Ischemia/reperfusion (I/R) damage is one of the main causes of acute kidney damage, and can develop in conditions such as hemorrhagic shock, partial nephrectomy, kidney transplant, and urological surgical procedures, causing organ loss due to temporary interruption of blood flow to the kidneys [1, 2]. Matrix metalloproteinase (MMP) is zinc and calcium-dependent neutral endopeptidase playing important roles in the regulation of cell-matrix composition that is responsible for the degradation of the extracellular matrix. MMPs are divided into six groups according to their structure and substrate specificities, and especially gelatinases (MMP-2 and MMP-9) in this group play an important role for Type IV collagen degradation, which is the main component of the basement membrane [7]. MMPs are basically regulated by three MAPK pathways, p38 MAPK, c-Jun N terminal kinase (JNK) and extracellular signal-regulated kinase (ERK) [9]. This pathway is activated p38 MAPK by the ROS. With the activation of this pathway, it has been shown in many studies that MMP-2 and MMP-9 are up-regulated [10, 11]
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