Abstract
Background Renal ischemia–reperfusion (I/R) injury plays an important role in the acute kidney injury. The pathogenetic mechanisms potential I/R injury is involved in apoptosis and inflammation. Epigallocatechin gallate (EGCG), a major constituent of green tea, has been shown to have anti-inflammatory and anti-apoptotic activities. This study aimed to explore the underlying effects and mechanisms of EGCG on renal I/R injury in a rat model.Materials and methodsWe induced renal I/R injury in SD rats by clamping the left renal artery for 45 min followed by 24-h reperfusion, along with a contralateral nephrectomy. We randomly allocated 30 rats to three groups (n = 10): sham group, IRI group, and EGCG group. We preconditioned rats intraperitoneally with EGCG (50 mg/kg) or vehicle (50 mg/kg) 45 min before inducing renal ischemia. We collected serum and kidneys at 24 h after reperfusion. Renal function and histologic damage were assessed. We also determined markers of inflammation and apoptosis in kidneys or serum.ResultsEGCG pretreatment can significantly reduce renal dysfunction, histologic change and the expression of tumor necrosis factor-α, IL-1β, IL-6, Bax and cleavage caspase 3 induced by I/R injury and increase the expression of Bax and caspase 3. Moreover, EGCG pretreatment can further induce the activation of p38 mitogen-activated protein kinase in kidney, with no influence on the expression of p38.ConclusionsEGCG treatment can decrease renal ischemia–reperfusion injury by suppressing inflammation and cell apoptosis. Thus, EGCG may represent a potential strategy to reduce renal I/R injury.
Highlights
Renal ischemia–reperfusion (I/R) injury, a main cause of acute renal failure, leads to unbelievably high morbidity and mortality and is common in those with trauma, shock, transplantation, renal resection, and so on [1]
Research shows that pathogenesis of renal I/R injury is involved in inflammation, cell apoptosis, necrosis, reactive oxygen species, and so on [2]
We demonstrated that Epigallocatechin gallate (EGCG) treatment at the concentration of 50 mg/kg significantly decreased I/R-induced renal dysfunction and histopathologic change as demonstrated by low Cr and Blood urea nitrogen (BUN) levels, degeneration tubular architecture, tubular cell swelling, tubular dilation, tubular necrosis and inflammatory cell infiltration
Summary
Renal ischemia–reperfusion (I/R) injury, a main cause of acute renal failure, leads to unbelievably high morbidity and mortality and is common in those with trauma, shock, transplantation, renal resection, and so on [1]. It is reported that inflammation and cell apoptosis play a vital role in renal I/R injury [3]. Mitogen-activated protein kinase (MAPK) is a traditional signal pathway that plays an important role in regulating NF-κB activation in renal ischemia–reperfusion injury [4]. NF-κB activation can induce inflammation and cell apoptosis [5]. Renal ischemia–reperfusion (I/R) injury plays an important role in the acute kidney injury. We determined markers of inflammation and apoptosis in kidneys or serum. Results EGCG pretreatment can significantly reduce renal dysfunction, histologic change and the expression of tumor necrosis factor-α, IL-1β, IL-6, Bax and cleavage caspase 3 induced by I/R injury and increase the expression of Bax and caspase 3. EGCG pretreatment can further induce the activation of p38 mitogen-activated protein kinase in kidney, with no influence on the expression of p38
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