ライフサイエンスコーパス: renal ischemia

1 njury and improved kidney function following renal ischemia.

2 t in the prevention or treatment of AKI from renal ischemia.

3 reserving kidney function during episodes of renal ischemia.

4 tive period, the most common cause of AKI is renal ischemia.

5 lar injury and organ dysfunction after acute renal ischemia.

6 iption of TNF-alpha and MCP-1 in response to renal ischemia.

7 MCP-1 by the proximal tubule in response to renal ischemia.

8 that are capable of mobilizing EPCs in acute renal ischemia.

9 therapeutic strategies for renal tumors and renal ischemia.

10 hat distant lung injury occurs rapidly after renal ischemia.

11 g injury develops after shock or visceral or renal ischemia.

12 s recently been reported to be induced after renal ischemia.

13 bradykinin, methacholine, or morphine before renal ischemia.

14 a, and inner medulla of rats after bilateral renal ischemia.

15 nhibits renal injury in a model of bilateral renal ischemia.

16 y the patterns of NOS activity in a model of renal ischemia.

17 ted acute renal failure in rats subjected to renal ischemia.

18 in the development of tubular obstruction in renal ischemia.

19 e 2 mg/kg dose of OKY-046 administered after renal ischemia.

20 exus and promotes early tubular injury after renal ischemia.

21 jecting these animals to 60 min of bilateral renal ischemia.

22 anti-G-CSFR 24 h prior to 22-min unilateral renal ischemia.

23 ue-Dawley rats after 45 minutes of bilateral renal ischemia.

24 rom the injury and mortality associated with renal ischemia.

25 ro-ischemia technique that eliminates global renal ischemia.

26 his system is profoundly perturbed following renal ischemia, a leading cause of acute kidney injury (

27 panies renal ischemia, it is unknown whether renal ischemia affects the production of antibodies by B

28 induction of ischemia in the mouse model of renal ischemia, an increase in intrarenal expression of

29 Rats were subjected to 60 min of bilateral renal ischemia and 6 h of reperfusion in the absence or

30 n results in pulmonary injury independent of renal ischemia and highlight the critical role of the ki

31 mobilized into the circulation by transient renal ischemia and home specifically to injured regions

32 osatetraenoic acid levels are elevated after renal ischemia and may protect against injury.

33 rine was related to the dose and duration of renal ischemia and preceded the appearance of other urin

34 ith SS-31 protected cristae membranes during renal ischemia and prevented mitochondrial swelling.

35 ation, play a crucial role in the process of renal ischemia and reperfusion (I/R) injury.

36 Cytoskeletal degradation occurs in warm renal ischemia and reperfusion and during hypothermia.

37 Renal ischemia and reperfusion injury causes loss of ren

38 a levels in Adora2b-deficient mice following renal ischemia and reperfusion.

39 7 on parenchymal cells promotes injury after renal ischemia and reperfusion.

40 wild-type (WT) littermate controls underwent renal ischemia and reperfusion.

41 trite anions may play a role in normothermic renal ischemia and reperfusion.

42 dergo a change in activity or function after renal ischemia and reperfusion.

43 f alpha-MSH inhibits acute lung injury after renal ischemia and to determine the early mechanisms of

44 Here, we developed a series of murine renal ischemia and transplant models to investigate sex-

45 A), or right nephrectomy with 60 min of left renal ischemia and treatment with inactive vehicle only

46 18 (mild IRI) or 22 min (moderate IRI) warm renal ischemia, and analyzed 24 h after reperfusion for

47 on animal survival after transient bilateral renal ischemia associated with severe AKI.

48 significant renal failure), suggesting that renal ischemia but not uremia is necessary for the apopt

49 lpha and that administration of xenon before renal ischemia can prevent acute renal failure.

50 erol did not raise hepatic FC/CE; unilateral renal ischemia did not alter contralateral renal FC/CE l

51 this procedure laparoscopically, namely warm renal ischemia during occlusion of the renal vascular pe

52 hemia and reperfusion) and then to 30 min of renal ischemia either 15 min (acute IPC) or 24 h (delaye

53 When rats were subjected to 45 min of renal ischemia, electrophoretic mobility shift assays of

54 Acute renal ischemia elicits an inflammatory response that may

55 y can now be safely performed without global renal ischemia, even for complex tumors.

56 Rats recovering from acute renal ischemia exhibit tubule loss and interstitial fibr

57 , wild-type (WT) and Gal-3-/- mice underwent renal ischemia followed by reperfusion (rIR).

58 nsgenic mice were subjected to 26 minutes of renal ischemia followed by reperfusion for 72 hours.

59 on from IRI induced by 27.5 min of bilateral renal ischemia, followed by 20 h of reperfusion (blood u

60 57BL/6), ARF was induced by 32 min bilateral renal ischemia, followed by reperfusion (I/R).

61 erexpressing (HBAC) mice underwent bilateral renal ischemia for 10 minutes.

62 Twenty-four hours after bilateral renal ischemia for 22.5 minutes, transgenic sickle mice

63 7BL/6 adult mice underwent standardized warm renal ischemia for 28 min after being injected with the

64 to male Wistar rats 30 min before bilateral renal ischemia for 45 min followed by reperfusion for up

65 s of the brain in mice by inducing bilateral renal ischemia for 60 min and studying the brains 24 h l

66 d-type and Adora2b-deficient mice undergoing renal ischemia for expression of a range of inflammatory

67 the hypothesis that cytokines released with renal ischemia have effects on other organ systems.

68 Renovascular disease leads to renal ischemia, hypertension, and eventual kidney failur

69 We examined the effect of renal ischemia in a transgenic mouse expressing human si

70 abbits (3.1-3.5 kg), with experimental focal renal ischemia in five kidneys.

71 Cardiac arrest (CA) causes renal ischemia in one-third of brain-dead kidney donors

72 nistered intravenously 24 and 48 hours after renal ischemia in rats.

73 APRF was induced by bilateral renal ischemia in situ (32 min), followed by reperfusion

74 a (TNF-alpha) and interleukin-1 (IL-1) after renal ischemia in the mouse.

75 olecule-1 mRNA were found in the heart after renal ischemia in the rat.

76 Thus, renal ischemia in this murine model induces more severe

77 study compared and contrasted the effects of renal ischemia in wild-type mice and mice deficient in c

78 study compared and contrasted the effects of renal ischemia in wild-type mice and mice deficient in N

79 study compared and contrasted the effects of renal ischemia in wild-type mice and mice deficient in T

80 ts against both kidney and lung damage after renal ischemia, in part, by inhibiting activation of tra

81 Functional changes in the heart 48 h after renal ischemia included increases in left ventricular en

82 Notably, renal ischemia induced a transient increase in cellular

83 Because renal ischemia induced by red blood cell sickling exacer

84 Transient renal ischemia induces both inflammatory and fibrotic pr

85 This study documents that renal ischemia induces dynamic changes in the molecular

86 vivo rat ischemic model to demonstrate that renal ischemia induces podocyte effacement with loss of

87 e assessed for delayed complications such as renal ischemia, infarct, urinoma, or tumor recurrence.

88 so found 48 h after an abbreviated period of renal ischemia insufficient to induce azotemia but not b

89 Renal ischemia is among the leading causes of acute kidn

90 Because renal ischemia is characterized by disruption of the ren

91 Renal ischemia is the result of a complex series of even

92 Global renal ischemia is thus eliminated.

93 nce of renal vasoconstriction and subsequent renal ischemia, is a common problem for which no proven

94 s known that tissue inflammation accompanies renal ischemia, it is unknown whether renal ischemia aff

95 Bilateral renal ischemia led to the expiration of 64% of wild-type

96 of chronic allograft nephropathy by causing renal ischemia mediated by vasoconstrictive metabolites

97 tected against the heightened sensitivity to renal ischemia observed in sickle mice, preventing ische

98 With bilateral renal ischemia of greater duration (22.5 minutes), and a

99 With bilateral renal ischemia of short or long duration, renal expressi

100 In AS160-knockout mice, the effects of renal ischemia on the distribution of Na(+),K(+)-ATPase

101 Mice subjected to renal ischemia or bilateral nephrectomy had moderate to

102 Mice underwent 32-min bilateral renal ischemia or identical sham operations.

103 studied 24 and 72 hours after 30 minutes of renal ischemia or sham operation.

104 subjected to 30 minutes of either unilateral renal ischemia or sham surgery.

105 Renal ischemia or the loss of blood flow to the kidneys

106 The impact of 40 minutes of unilateral renal ischemia plus reflow (3 to 6 days) on mouse cortic

107 cted into wild-type C57BL/6 mice 24 h before renal ischemia, protect mice from developing renal IRI.

108 Renal ischemia rapidly activated kidney and lung nuclear

109 ul interventions in the preclinical setting, renal ischemia reperfusion (IR) injury remains a major p

110 gher in renalase-deficient mice subjected to renal ischemia reperfusion compared with wild-type mice.

111 a clinically relevant swine model of severe renal ischemia reperfusion injury (IRI) induced by hemor

112 Renal ischemia reperfusion injury (IRI) is associated wi

113 ed differential effects of these isoforms in renal ischemia reperfusion injury (IRI) using inducible

114 or metformin in C57BL/6 mice challenged with renal ischemia reperfusion injury (IRI), treated before

115 have been implicated in the pathogenesis of renal ischemia reperfusion injury (IRI).

116 role for CD4(+) cells in the pathogenesis of renal ischemia reperfusion injury (IRI).

117 loss of function in the absence of IgM after renal ischemia reperfusion injury and cardiac allograft

118 Here, mice subjected to renal ischemia reperfusion injury had significantly lowe

119 Renal ischemia reperfusion injury triggers complement ac

120 The protective effect on renal ischemia reperfusion injury was not observed using

121 ded to further examine the effects of HMP on renal ischemia reperfusion injury.

122 e in rabbits, and there were too few data on renal ischemia reperfusion injury.

123 asma NE levels increased significantly after renal ischemia reperfusion injury.

124 osis, suggesting that it may protect against renal ischemia reperfusion injury.

125 en investigated in cerebral, myocardial, and renal ischemia reperfusion injury; helium and xenon have

126 In a study of renal ischemia reperfusion, cysteamine therapy initiated

127 ith broad-spectrum antibiotics and performed renal ischemia-reperfusion (I/R) injury in mice.

128 BACKGROUND Following allotransplantation, renal ischemia-reperfusion (I/R) injury initiates a seri

129 Renal ischemia-reperfusion (I/R) injury is a major cause

130 and angiogenesis were evaluated in mice with renal ischemia-reperfusion (I/R) injury.

131 nized to be important in the pathogenesis of renal ischemia-reperfusion (I/R) injury.

132 l cell (EC) activation plays a major role in renal ischemia-reperfusion (I/R) injury.

133 Renal ischemia-reperfusion (I/R) is a major contributor

134 BL/6 mice were subjected to 30 min bilateral renal ischemia-reperfusion (I/R) to induce AKI.

135 sphate receptor 1 (S1P(1)R) protects against renal ischemia-reperfusion (IR) injury and inflammation,

136 del of enhanced remote atherosclerosis after renal ischemia-reperfusion (IR) injury and investigated

137 of wild-type mice with retinoic acid before renal ischemia-reperfusion blunted the induction of Nur7

138 Renal ischemia-reperfusion caused a rapid decrease in se

139 tophagy was induced in kidney tissues during renal ischemia-reperfusion in mice.

140 e pharmacologic strategy proposed to prevent renal ischemia-reperfusion injuries and delayed graft fu

141 Using rat renal ischemia-reperfusion injury (IRI) as a model of ac

142 In vivo, more severe renal ischemia-reperfusion injury (IRI) associated with

143 Severe renal ischemia-reperfusion injury (IRI) can lead to acut

144 d during the process of tubular repair after renal ischemia-reperfusion injury (IRI) in male Sprague

145 plement regulators CD55 and CD59 exacerbates renal ischemia-reperfusion injury (IRI) in mouse models,

146 Renal ischemia-reperfusion injury (IRI) is a common comp

147 Renal ischemia-reperfusion injury (IRI) is a feature of

148 However, its role in renal ischemia-reperfusion injury (IRI) is controversial

149 Renal ischemia-reperfusion injury (IRI) leads to acute k

150 Renal ischemia-reperfusion injury (IRI) predictably caus

151 To examine the role of the inflammasome in renal ischemia-reperfusion injury (IRI) we also tested i

152 NMP may allow directed pharmacomodulation of renal ischemia-reperfusion injury (IRI) without the need

153 s (Tregs) can suppress immunologic damage in renal ischemia-reperfusion injury (IRI), but the isolati

154 Following renal ischemia-reperfusion injury (IRI), resolution of i

155 , these animals were remarkably resistant to renal ischemia-reperfusion injury (IRI), showing signifi

156 analogue (LIMM102) in a preclinical model of renal ischemia-reperfusion injury (IRI)-induced AKI.

157 the renal microvasculature is a hallmark of renal ischemia-reperfusion injury (IRI)-mediated AKI.

158 renal protective effect of A(2A) agonists in renal ischemia-reperfusion injury (IRI).

159 tream from protein kinase C (PKC) may reduce renal ischemia-reperfusion injury and confer renal graft

160 mportantly, CK-666 significantly ameliorated renal ischemia-reperfusion injury and ferroptosis in ren

161 assessed in the kidneys of 6 mice undergoing renal ischemia-reperfusion injury and in 6 control kidne

162 trin-1 acting through UNC5B receptor reduces renal ischemia-reperfusion injury and its associated ren

163 We used murine renal ischemia-reperfusion injury and kidney organoids (

164 that IL24 is upregulated in the kidney after renal ischemia-reperfusion injury and that tubular epith

165 es acute renal failure, and the hallmarks of renal ischemia-reperfusion injury are inflammation, apop

166 endothelial Phd2 ablation protected against renal ischemia-reperfusion injury by suppressing the exp

167 introduction to exploratory analysis; 5) rat renal ischemia-reperfusion injury case study; (6) linear

168 Renal ischemia-reperfusion injury causes acute renal fai

169 In an established mouse model of renal ischemia-reperfusion injury characterized by apopt

170 zed with a foreign antigen 24-96 hours after renal ischemia-reperfusion injury developed increased le

171 Renal ischemia-reperfusion injury did not cause amplific

172 omes following a single episode of bilateral renal ischemia-reperfusion injury in female C57BL/6 mice

173 that dehydroepiandrosterone protects against renal ischemia-reperfusion injury in male rats.

174 ce renal IL-11 expression or protect against renal ischemia-reperfusion injury in mice lacking the re

175 fects in inhibiting ferroptosis and reducing renal ischemia-reperfusion injury in mice.

176 inhibitors could provide protection against renal ischemia-reperfusion injury in the rat in vivo.

177 Pretreatment with CCPA protected against renal ischemia-reperfusion injury in wild-type mice, but

178 Renal ischemia-reperfusion injury induced hepatosplenic

179 Renal ischemia-reperfusion injury is an important contri

180 Renal ischemia-reperfusion injury is mediated by a compl

181 models of ischemic renal injury: an in situ renal ischemia-reperfusion injury model (predominantly w

182 Results of this study in a renal ischemia-reperfusion injury model allow phenotype

183 out mice lacking periostin expression in the renal ischemia-reperfusion injury model, and primary cul

184 ive effect of amniotic fluid stem cells in a renal ischemia-reperfusion injury model.

185 nchronization modulation electric field to a renal ischemia-reperfusion injury mouse model preserved

186 d a mouse model to investigate the effect of renal ischemia-reperfusion injury on systemic iron homeo

187 Mechanisms of renal ischemia-reperfusion injury remain unresolved, and

188 In summary, renal ischemia-reperfusion injury results in profound al

189 s an endogenous protective mechanism against renal ischemia-reperfusion injury through inhibition of

190 lar injury in kidneys subjected to bilateral renal ischemia-reperfusion injury was more severe in the

191 Renal ischemia-reperfusion injury with bilateral renal p

192 Six hours after induction of renal ischemia-reperfusion injury, amniotic fluid stem c

193 reduced netrin-1-mediated protection against renal ischemia-reperfusion injury, and it increased mono

194 rophages rapidly infiltrate the kidney after renal ischemia-reperfusion injury, however specific mole

195 nd neutrophils to kidney in a mouse model of renal ischemia-reperfusion injury, however this activity

196 In an established murine model of renal ischemia-reperfusion injury, intravenous NGAL admi

197 human amniotic fluid stem cells in rats with renal ischemia-reperfusion injury, mainly by mitogenic,

198 After renal ischemia-reperfusion injury, MFG-E8 mRNA and prote

199 ing in plasma samples from rats subjected to renal ischemia-reperfusion injury, pigs subjected to ren

200 a nitrogen and serum creatinine in rats with renal ischemia-reperfusion injury, providing evidence fo

201 educes inflammation to mediate protection in renal ischemia-reperfusion injury, suggesting that hepci

202 In a mouse model of renal ischemia-reperfusion injury, tempol-folate reduced

203 ion, although both C3a and C5a contribute to renal ischemia-reperfusion injury, the pathogenic role o

204 -, or C3aR/C5aR-deficient mice and models of renal ischemia-reperfusion injury, we found that deficie

205 Using a chimeric mouse model for renal ischemia-reperfusion injury, we found that NLRX1 p

206 deficiency of endothelial HIF-2 exacerbated renal ischemia-reperfusion injury, whereas inactivation

207 In a model of renal ischemia-reperfusion injury, xenon provided morpho

208 econditional HIF activation protects against renal ischemia-reperfusion injury, yet the mechanisms in

209 ce, systemic iron overload protected against renal ischemia-reperfusion injury-associated sterile inf

210 eukocytes contributes to the pathogenesis of renal ischemia-reperfusion injury.

211 l cells or circulating leukocytes attenuated renal ischemia-reperfusion injury.

212 of preconditioning in mice before and after renal ischemia-reperfusion injury.

213 G-E8 can be developed as novel treatment for renal ischemia-reperfusion injury.

214 whether administration of MFG-E8 attenuates renal ischemia-reperfusion injury.

215 ophil infiltration in a 7 day mouse model of renal ischemia-reperfusion injury.

216 subjected hif1a(+/-) and hif2a(+/-) mice to renal ischemia-reperfusion injury.

217 eptor shown to contribute to fibrogenesis in renal ischemia-reperfusion injury.

218 n uninjured kidney or intra-arterially after renal ischemia-reperfusion injury.

219 (WT) and CD47(-/-) mice were challenged with renal ischemia-reperfusion injury.

220 3 hours) treatment with necrostatin-1 during renal ischemia-reperfusion injury.

221 er validated in a model of ER-stress-induced renal ischemia-reperfusion injury.

222 ytokines are involved in the pathogenesis of renal ischemia-reperfusion injury.

223 nd the inflammatory response after sublethal renal ischemia-reperfusion injury.

224 , mediated by C1 neurons: protection against renal ischemia-reperfusion injury.

225 f talin-mediated activation of integrins for renal ischemia-reperfusion injury.

226 stress is implicated in the pathogenesis of renal ischemia-reperfusion injury.

227 ies is a major cause of tissue damage during renal ischemia-reperfusion injury.

228 alpha12 activation and protects mice against renal ischemia-reperfusion injury.

229 (L325R) in myeloid cells were protected from renal ischemia-reperfusion injury.

230 pecific ablation of PHD2 in a mouse model of renal ischemia-reperfusion injury.

231 We used the renal ischemia-reperfusion model to investigate the role

232 After induction of AKI in mice by renal ischemia-reperfusion or bilateral nephrectomy, sma

233 stitution of SULT1E1 expression to bilateral renal ischemia-reperfusion or sham surgery, either in th

234 tion of recombinant netrin-1 before or after renal ischemia-reperfusion reduced kidney injury, apopto

235 blasts and renal proximal tubular cells, and renal ischemia-reperfusion to induce stress in mice.

236 It is also overexpressed after renal ischemia-reperfusion, an event that induces kidney

237 After renal ischemia-reperfusion, Nurr77-deficient mice exhibi

238 Exogenous hepcidin treatment prevented renal ischemia-reperfusion-induced changes in iron homeo

239 bule-specific deletion of Drp1 prevented the renal ischemia-reperfusion-induced kidney injury, inflam

240 tic benefit in models of ischemic stroke and renal ischemia-reperfusion.

241 Renal ischemia/reperfusion (I/R) can induce acute kidney

242 eness in the setting of preceding unilateral renal ischemia/reperfusion (I/R) in mouse AKI model.

243 Renal ischemia/reperfusion (I/R) injury is a common clin

244 Renal ischemia/reperfusion (I/R) injury is a major cause

245 cohydrolase (PARG) in the pathophysiology of renal ischemia/reperfusion (I/R) injury is not known.

246 ium nitrite administration in a rat model of renal ischemia/reperfusion (I/R) injury.

247 In rats, following renal ischemia/reperfusion (I/R), there was a rapid and

248 Renal FoxM1 expression increased after renal ischemia/reperfusion (I/R)-induced AKI in mouse ki

249 ctivated within the tubulointerstitium after renal ischemia/reperfusion (I/R).

250 ge of mitochondria in experimental models of renal ischemia/reperfusion and cisplatin-induced nephrot

251 red in proximal tubular cells in mice during renal ischemia/reperfusion and cisplatin-induced nephrot

252 ess the role of Nlrp3 in the repair phase of renal ischemia/reperfusion and investigate the relative

253 rate of epithelial cell proliferation after renal ischemia/reperfusion in aged mice but also increas

254 owever, the pathogenic mechanisms underlying renal ischemia/reperfusion injury (IRI) are not fully de

255 at polyclonal natural IgM protects mice from renal ischemia/reperfusion injury (IRI) by inhibiting th

256 Here, using a murine renal ischemia/reperfusion injury (IRI) model, we show t

257 ype littermates were subjected to unilateral renal ischemia/reperfusion injury (IRI) or unilateral ur

258 e tubulointerstitial damage, including acute renal ischemia/reperfusion injury (IRI).

259 s poorly defined, the role of cathepsin G in renal ischemia/reperfusion injury was tested.

260 In mice, Bif-1 bound prohibitin-2 during renal ischemia/reperfusion injury, and Bif-1-deficiency

261 by chloroquine and 3-methyladenine worsened renal ischemia/reperfusion injury, as indicated by renal

262 se results suggest that CSE protects against renal ischemia/reperfusion injury, likely by modulating

263 Similarly, in a rat model of renal ischemia/reperfusion injury, SAR247799 preserved r

264 ole for Galpha12 activation during bilateral renal ischemia/reperfusion injury.

265 ctional kidney changes, and mortality during renal ischemia/reperfusion injury.

266 ssue pathology and subsequent fibrosis after renal ischemia/reperfusion injury.

267 l tissue damage in an ROS-dependent model of renal ischemia/reperfusion injury.

268 mimic sepsis), cisplatin administration, or renal ischemia/reperfusion injury.

269 ed with increased damage and mortality after renal ischemia/reperfusion injury.

270 We conclude: (a) alpha-MSH protects against renal ischemia/reperfusion injury; and (b) it may act, i

271 Renal ischemia/reperfusion is a major cause of acute kid

272 chemotactic protein-1, and P-selectin, after renal ischemia/reperfusion, exacerbating apoptosis and f

273 by unilateral ureteral obstruction (UUO) or renal ischemia/reperfusion, which was accompanied by a s

274 roliferation and modifies the pathology in a renal ischemia/reperfusion-injury disease model, via its

275 ice from death and hypothermia in sepsis and renal ischemia/reperfusion.

276 osis factor-alpha at early time points after renal ischemia/reperfusion.

277 he alternative splicing during the course of renal ischemia/reperfusion.

278 l artery contraction by AT1R activation with renal ischemia representing a key permissive factor and

279 allin in various renal compartments; and (2) Renal ischemia results in differential accumulation of h

280 Renal ischemia results in distant effects and the altera

281 Examination of graded times of renal ischemia revealed a direct correlation between the

282 ed, FVB/NJ mice that were subjected to acute renal ischemia showed a transient surge in UA level in t

283 Thirty minutes of renal ischemia significantly elevated serum creatinine i

284 maintaining blood flow during recovery from renal ischemia, the observed decrease in NOS activity ma

285 During the repair phase of transient renal ischemia, these cells entered the cell cycle and t

286 Mice were subjected to renal ischemia treated with vehicle or alpha-MSH.

287 IL-6 that was produced in response to renal ischemia was maladaptive because transgenic knocko

288 Three days later, renal ischemia was produced by cross-clamping the left r

289 present study, an animal model of bilateral renal ischemia was used to test the hypothesis that cyto

290 ion of metabolic stress, which occurs during renal ischemia, we infected immortalized and primary pro

291 factors are simultaneously activated during renal ischemia, which might account for observed differe

292 a greater rise in blood urea nitrogen after renal ischemia, while stem cell infusion after bone marr

293 enal genes that are induced very early after renal ischemia, whose protein products might serve as no

294 6), consisting of 3 cycles of 30 seconds of renal ischemia with 30 seconds intervening reperfusion.

295 C57BL/6 mice were subjected to 30 min of renal ischemia, with or without pretreatment with 1,3-di