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Purpose of complex renal surgery, renal transplantation, renal parenchyma incision lithotomy of partial nephrectomy for renal tumors, vascular surgery, aortic repair surgery is required to block the renal blood flow caused by renal ischemia-reperfusion ( ischemia-reperfusion, I / R) injury. Room temperature, blocking the renal blood flow for more than 40 min, will lead to acute renal failure, I / R injury is also a kidney transplant, the main factors affecting early functional recovery and long-term survival of the transplanted kidney. How to prevent and reduce I / R injury, is the renoprotective the main subject. In this study, preliminary experiments were successfully prepared rat kidney I / R injury model rat kidney I / R injury ischemia (ischemic postconditioning, IPo) model, post-processing observed ulinastatin (ulinastain, U), pretreatment ischemic preconditioning (the ischemic preconditioning IP) IPo by scavenging free radicals, enhance the activity of SOD, reduce lipid peroxidation, inhibition of apoptosis and reduce rat I / R renal injury. Ischemia-reperfusion injury is caused by many factors complex pathophysiological process sublethal ischemic injury can lead to cell damage, and more reperfusion intracellular source of reactive oxygen species and aggravated the injury; addition, inflammatory the formation of the precursor of the medium, macrophages, neutrophils, and the aggregation and activation of lymphocytes is further aggravate the injury; Microcirculation of obstruction can lead to the formation of non-perfused region and causing ischemic injury. Protection measures for a single medium or mechanisms to achieve the desired protective effect is very difficult. This study on the basis of previous experiments explore Ischemic preconditioning, ischemic postconditioning ulinastatin combined with the effect and mechanism of I / R injury in rat kidney. Protection for clinical ischemic reperfusion injury kidney provide a theoretical basis for the establishment of a new, more reasonable way to reduce kidney damage, protection of renal function. 36 male Sprague-Dawley rats were randomly divided into 6 groups (n = 6), sham group (S group), ischemia-reperfusion group (I / R group), ischemic preconditioning combined treatment group (IP IPo group ), ulinastatin ischemic preconditioning group (U IP group), the ulinastatin the small joint ischemia after the treatment group the (U IPo group), ulinastatin ischemic preconditioning in the combined treatment group (U IP the group IPo). 10% chloral hydrate 3 ml / kg intraperitoneal injection of anesthesia, clamping bilateral renal pedicle 45 min, 6 h reperfusion renal I / R injury model was prepared. No damage arterial clipping the bilateral the renal pedicle kidneys color becomes dark red to confirm renal vascular occlusion, resulting in bilateral renal ischemia for 45 min, release the artery clip, kidney recovery from dark red red Seji can confirm that the restoration of blood flow, occlusion and release the renal pedicle intraperitoneal injection of Ringer's solution 20 ml / kg. S group underwent open to free both kidneys isolated bilateral renal pedicle occlusion, wound with saline gauze covering exposed 45 min for renal ischemia treatment; I / R group clipping bilateral renal pedicle missing artery clip; blood 45 min after the release IP IPO group first given clamping bilateral renal pedicle ischemia for 5 min before ischemia and reperfusion 5 min, repeated three times, clamping bilateral renal pedicle ischemia for 45 min after perfusion 10 s, the ischemia 10 s, repeated three times, and then restore blood perfusion 6 h; U IP Group: 30 min before ischemia by intravenous injection of ulinastatin D 2 × 104 U / kg, clamping bilateral renal pedicle 5 min of ischemia and reperfusion 5 min, repeated three times, giving the clamping bilateral renal pedicle after 45 min of ischemia, and then restore perfusion 6h; injected via the tail vein 30 min before ischemia U IPo was group ulinastatin × 104 U / kg, clamping bilateral renal pedicle after 45 min of ischemia, reperfusion 10 s, 10 s of ischemia, repeated three times, and then restore blood perfusion 6 h; U IP IPo was group 30 min before ischemia via the tail Intravenous ulinastatin 2 × 104 U / kg, more than operating the same IP IPo group. The rats were sacrificed 6 h reperfusion, enzymatic determination of the level of serum creatinine (Cr), picric acid in addition to protein determination of blood urea nitrogen (BUN) level; radioimmunoassay determination of urinary α1-microglobulin (α1-MG) level ; thiobarbituric acid (TBA) method for determination of renal malondialdehyde (MDA), and xanthine oxidase, superoxide dismutase (SOD) activity was measured; situ terminal deoxynucleotidyl transferase labeling (TUNEL apoptotic cells) in renal tissue was detected by immunohistochemistry (SP), calculated the apoptotic index the (apopatic index, AI); observed by the kidney tissue of apoptosis-related protein Bcl-2, Bax and Caspase-3 expression, calculated protein positive staining index (positive index, PI); hematoxylin - eosin (HE) staining, renal histopathological changes observed in the light microscope. Results are compared with S group, 6 h reperfusion, I / R group, IP IPo group, U IP group, U IPo group, serum Cr and BUN concentration of U IP IPo was group was significantly higher (P lt; 0.05), urinary α1 lower (P lt; 0.05)-MG content increased (P lt; 0.05), kidney tissue SOD activity and MDA content increased (P lt; 0.05), the expression of Bcl-2 protein PI decreased (P lt; 0.05), Bax protein PI l high (P lt; 0.05), elevated caspase-3 protein PI (P lt; 0.05) increase in renal tissue apoptosis index (AI) (P lt; 0.05), the pathological damage is obvious. Compared with the I / R group, IP IPo group, U IP group, U IPo group, serum Cr and BUN concentration of U IP IPo was group decreased significantly (P lt; 0.05), α1-MG content in urine reduce (P lt; 0.05) renal tissue SOD activity increased (P lt; 0.05), the content of MDA decreased (P lt; 0.05), the expression of Bcl-2 protein PI increased (P lt; 0.05), Bax protein PI lower (P lt; 0.05), Caspase 3 protein PI lower (P lt; 0.05), decrease in renal tissue apoptosis index (AI) (P lt; 0.05), and significantly reduce the light microscope, renal tissue injury. The the U IP group the, U IP IPo urinary α1-MG decreased (P lt; 0.05), kidney tissue SOD activity lower (P lt; 0.05), decrease in renal tissue apoptosis index (AI) (P lt; 0.05) ; U IP group U IPO renal tissue apoptosis index (AI) decreased (P lt; 0.05). Compared with the IP IPo group the U IP IPo was group Bcl-2 protein PI increased (P lt; 0.05). Compared with the U IPo group the U IP IPo was group Bcl-2 protein PI increased (P lt; 0.05). Other indexes the the groups of IP IPo, U IP group, U IPo group, U IP IPo was group difference was not statistically significant (P gt; 0.05). Conclusion 1 ischemic preconditioning combined with post-processing ulinastatin D joint ischemic preconditioning, processing and Ukrainian Division of the Ukrainian Division his Ding Joint postischemic D ischemic preconditioning combined treatment may reduce the rat kidney I / R injury and improve kidney function. Its main mechanism may scavenge free radicals directly and through enhanced SOD activity, reduce lipid peroxidation, inhibition of apoptosis related. 2 ischemic preconditioning combined post-processing, ulinastatin combined with ischemic preconditioning, ulinastatin the small joint ischemia after treatment and ulinastatin the ischemic preconditioning joint after processing has a similar renoprotective effect Ulinastatin, He Ding, the protective effect of ischemic preconditioning combined treatment is better.
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