Protection of endotoxin-induced oxidative renal tissue damage of rats by vitamin E or/and EGb 761 treatment

Iron overload and enhanced hydroxyl radical (•OH) formation have been implicated as the causative factors of oxidative stress in different organs. Both pro-oxidant and anti-oxidant properties have been reported for nitric oxide (NO) in iron-mediated tissue injury. To determine the contribution of NO to iron-induced renal injury, eight groups of rats (eight in each group) were studied as follows: control (normal saline), L-Arg (L-arginine as a substrate of NO synthase, 400 mg/kg), L-NAME (an inhibitor of NO synthase, 8 mg/kg), Fe (iron dextran, 600 mg/kg), DFO (deferroxamine as a chelator of iron, 150 mg/kg), Fe+L-Arg, Fe+L-NAME, DFO+L-Arg. Twenty-four hours after the injections, blood samples were taken and kidneys removed for biochemical analysis. Plasma creatinine and urea were used to stimulate renal function. Renal tissue and plasma vitamin E levels, the most important endogenous fat soluble antioxidant, were measured by HPLC and UV detection. In this study, renal function was markedly reduced in the Fe group compared to controls (creatinine, 1.02± 0.05 mg/dL versus 0.78±0.04 P <0.05; urea, 49.59±1.69 mg/dL versus 40.75±0.86, P <0.01). Vitamin E levels were significantly lower in the Fe group compared to controls (plasma P <0.01; renal tissue P <0.05). Administration of L-Arg to Fe-treated groups prevented these reductions. L-NAME increased iron-induced toxicity significantly, demonstrated by further reduction in the vitamin E levels and renal function compared to the Fe group alone. We concluded that NO plays an important role in protecting the kidney from iron-induced nephrotoxicity. NO synthase blockade enhances iron-mediated renal toxicity in this model.

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Mesenteric Lymph Drainage Alleviates Acute Kidney Injury Induced by Hemorrhagic Shock without Resuscitation

The Scientific World JOURNAL ◽

10.1155/2014/720836 ◽

2014 ◽

Vol 2014 ◽

pp. 1-8 ◽

Cited By ~ 2

Author(s):

Zi-Gang Zhao ◽

Hong-Xia Zhu ◽

Li-Min Zhang ◽

Yu-Ping Zhang ◽

Chun-Yu Niu

Keyword(s):

Acute Kidney Injury ◽

Hemorrhagic Shock ◽

Tissue Damage ◽

Kidney Injury ◽

Renal Tissue ◽

Intercellular Adhesion Molecule ◽

Intercellular Adhesion Molecule 1 ◽

Lymph Drainage ◽

Mesenteric Lymph ◽

2,3 Dpg

This study aimed to investigate the effect of mesenteric lymph drainage on the acute kidney injury induced by hemorrhagic shock without resuscitation. Eighteen male Wistar rats were randomly divided into sham, shock, and drainage groups. The hemorrhagic shock model (40 mmHg, 3 h) was established in shock and drainage groups; mesenteric lymph drainage was performed from 1 h to 3 h of hypotension in the drainage group. The results showed that renal tissue damage occurred; the levels of urea, creatinine, and trypsin in the plasma as well as intercellular adhesion molecule-1 (ICAM-1), receptor of advanced glycation end-products (RAGE), tumor necrosis factor-α(TNF-α), malondialdehyde (MDA), lactic acid (LA), and 2,3-DPG in the renal tissue were increased in the shock group after 3 h of hypotension. Mesenteric lymph drainage lessened the following: renal tissue damage; urea and trypsin concentrations in the plasma; ICAM-1, RAGE, TNF-α, MDA, and LA levels in the renal tissue. By contrast, mesenteric lymph drainage increased the 2,3-DPG level in the renal tissue. These findings indicated that mesenteric lymph drainage could relieve kidney injury caused by sustained hypotension, and its mechanisms involve the decrease in trypsin activity, suppression of inflammation, alleviation of free radical injury, and improvement of energy metabolism.

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Renal Tissue Damage After Experimental Pyelonephritis: Role of Anti-Oxidants and Selective Cyclooxygenase-2 Inhibitors

Journal of Pediatric Urology ◽

10.1016/j.jpurol.2009.02.012 ◽

2009 ◽

Vol 5 ◽

pp. S22

Author(s):

Serhat Gurocak ◽

Iyimser Ure ◽

Ahmet Cumaoglu ◽

Ipek Isik Gonul ◽

Ilker Sen ◽

...

Keyword(s):

Tissue Damage ◽

Renal Tissue ◽

Cyclooxygenase 2 ◽

Experimental Pyelonephritis ◽

Cyclooxygenase 2 Inhibitors

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Protective effect of hydroalcoholic extract of tribulus terrestris on cisplatin induced renal tissue damage in male mice

International Journal of Preventive Medicine ◽

10.4103/2008-7802.151817 ◽

2015 ◽

Vol 6 (1) ◽

pp. 11 ◽

Cited By ~ 7

Author(s):

Ali Ghanbari ◽

Amir Raoofi ◽

Mozafar Khazaei

Keyword(s):

Protective Effect ◽

Tissue Damage ◽

Renal Tissue ◽

Tribulus Terrestris ◽

Male Mice ◽

Hydroalcoholic Extract

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Age-dependent shifts in renal response to injury relate to altered BMP6/CTGF expression and signaling

AJP Renal Physiology ◽

10.1152/ajprenal.00324.2016 ◽

2016 ◽

Vol 311 (5) ◽

pp. F926-F934 ◽

Cited By ~ 8

Author(s):

Lucas L. Falke ◽

Hiroshi Kinashi ◽

Amelie Dendooven ◽

Roel Broekhuizen ◽

Reinout Stoop ◽

...

Keyword(s):

Growth Factor ◽

Tissue Damage ◽

Transforming Growth Factor ◽

Transforming Growth Factor Β ◽

Renal Tissue ◽

Tissue Growth ◽

Bmp Signaling ◽

Obstructive Nephropathy ◽

Young Mice

Age is associated with an increased prevalence of chronic kidney disease (CKD), which, through progressive tissue damage and fibrosis, ultimately leads to loss of kidney function. Although much effort is put into studying CKD development experimentally, age has rarely been taken into account. Therefore, we investigated the effect of age on the development of renal tissue damage and fibrosis in a mouse model of obstructive nephropathy (i.e., unilateral ureter obstruction; UUO). We observed that after 14 days, obstructed kidneys of old mice had more tubulointerstitial atrophic damage but less fibrosis than those of young mice. This was associated with reduced connective tissue growth factor (CTGF), and higher bone morphogenetic protein 6 (BMP6) expression and pSMAD1/5/8 signaling, while transforming growth factor-β expression and transcriptional activity were no different in obstructed kidneys of old and young mice. In vitro, CTGF bound to and inhibited BMP6 activity. In summary, our data suggest that in obstructive nephropathy atrophy increases and fibrosis decreases with age and that this relates to increased BMP signaling, most likely due to higher BMP6 and lower CTGF expression.

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