Picroliv preconditioning protects the rat liver against ischemia–reperfusion injury

Singh, Anoop; Mani, Haresh; Seth, Pankaj; Gaddipati, Jaya P.; Kumari, Ranjana; Banuadha, Krishna K; Sharma, Shikha; Kulshreshtha, D. K.; Maheshwari, Radha K.

doi:10.1016/s0014-2999(00)00146-1

Cited by 37 publications

(18 citation statements)

References 34 publications

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“…Thus, consequences of the attack of biomolecules by ROS, such as lipid peroxidation, could result, thereby, in altering the structure of biological membranes. Research on animal and clinical studies have shown that there is a close relationship between a lipid peroxidative reaction and secondary pathological changes following reperfusion period [11]. In the present study, the levels of MDA, an end product of lipid peroxidation, are significantly increased in the I/R group.…”

Section: Discussionsupporting

confidence: 55%

Erdosteine Improves Oxidative Damage in a Rat Model of Renal Ischemia-Reperfusion Injury

Gürel

Armutçu²,

Cihan³

et al. 2004

Eur Surg Res

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The aim of the present study was to determine the effects of erdosteine, a new antioxidant and anti-inflammatory agent, on lipid peroxidation, neutrophil infiltration, and antioxidant enzyme activities in a rat model of renal ischemia-reperfusion (I/R) injury. Twenty-eight rats were divided into three groups: sham operation, I/R, and I/R plus erdosteine groups. After the experimental procedure, rats were sacrificed and kidneys were removed and prepared for malondialdehyde (MDA) levels, myeloperoxidase (MPO), xanthine oxidase (XO), catalase (CAT) and superoxide dismutase (SOD) activities. MDA level, MPO and XO activities were significantly increased in the I/R group. On the other hand, SOD and CAT activities were found to be decreased in the I/R group compared to the sham group. Pretreatment with erdosteine significantly diminished tissue MDA level, MPO and XO activities. Our data support a role for erdosteine in attenuation in renal damage after I/R injury of the kidney, in part at least by inhibition of neutrophil sequestration and XO activity.

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Section: Discussionsupporting

confidence: 55%

Erdosteine Improves Oxidative Damage in a Rat Model of Renal Ischemia-Reperfusion Injury

Gürel

Armutçu²,

Cihan³

et al. 2004

Eur Surg Res

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“…However, in accordance with other investigators, we detected only a few apoptotic hepatocytes in an NHBD model (warm ischemia, cold storage and subsequent reperfusion) [15]. In contrast to our results, other studies have shown a large amount of apoptotic hepatocytes after warm ischemia and following in vivo perfusion [9,10,16,26,35,36]. One explanation might be that we used an isolated organ reperfusion which does not include any ligands or apoptosis inducing factors, which in contrast are present during blood perfusion.…”

Section: Discussionsupporting

confidence: 89%

“…Warm ischemia of the liver in vivo and subsequent reperfusion induces apoptosis in hepatocytes [9,10,26,35,36]. Hence, hepatocytes are highly sensitive to induction of apoptosis through the Fas system [18, 23,24], which plays an outstanding role in various diseases of the liver [18, 20-22, 37, 38].…”

Section: Discussionmentioning

confidence: 99%

“…The Fas receptor, one of the tumor necrosis factors (TNFs) and a potent inducer of apoptosis in hepatocytes, is involved in numerous liver diseases, for example viral hepatitis and acute liver failure [18][19][20][21][22][23][24][25]. Other investigators have shown that inhibition of apoptosis after warm ischemia by an antioxidant reduced the amount of Fas mRNA in the liver [26]. A prolonged warm ischemia may lead to upregulation of the Fas receptor in liver tissues [10].…”

Section: Introductionmentioning

confidence: 99%

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Fas Receptor Is Upregulated in Livers from Non-Heart-Beating Donors

et al. 2001

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Cell injury in livers from non-heart-beating donors (NHBDs) is not only caused by necrosis, but it is increasingly being recognized that apoptotic transformation contributes to postischemic cell death. It remains unclear which pathways lead to apoptosis. We suggested that apoptosis in NHBD livers might be mediated by the Fas receptor. Therefore the aim of our study was the detection and quantification of the Fas receptor, Fas mRNA and apoptosis in NHBD livers. Livers of male Wistar rats were harvested either from heart-beating donors (control, n = 15) or 30 min after cardiac arrest from NHBDs (n = 15). All livers were stored in University of Wisconsin solution for 24 h at 4°C, and reperfused using a recirculating model with oxygenated Krebs-Henseleit buffer for 120 min at 37°C. Conventional signs of cell damage, such as enzyme release and bile production, showed an elevated nonspecific cell injury in NHBD livers. The immunohistochemical staining of Fas antigen expression revealed a 7% rate of Fas receptor-expressing hepatocytes in the control group, but a considerable increase up to 38% in the NHBD group. No Fas antigen expression was detected on sinusoidal endothelial cells. Real-time RT-PCR detected an approximately eightfold elevated concentration of Fas mRNA transcripts in NHBD livers. We conclude that upregulation of the Fas receptor on hepatocytes in NHBDs will prime these cells to eventually undergo apoptosis upon reperfusion in vivo. Therefore, therapeutic modulation of the Fas pathway must be considered as a new strategy in order to additionally protect NHBD livers which are otherwise prone to parenchymal apoptosis.

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“…Immunohistochemical staining was performed on paraffin sections of treated and control wounds for various growth factors as described earlier [22]. Sections were taken on aminoalkylsilanecoated slides (Sigma Diagnostics, St. Louis, Mo., USA).…”

Section: Immunohistochemical Localization Of Bfgf and Tgf-ßmentioning

confidence: 99%

Enhancement of Wound Healing by Shikonin Analogue 93/637 in Normal and Impaired Healing

Mani¹,

Sidhu²,

Singh³

et al. 2003

Skin Pharmacol Physiol

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Wound healing is a complicated biological process, which involves interactions of multiple cell types, various growth factors, their mediators and the extracellular matrix proteins. In this study, we evaluated the effects of shikonin analogue 93/637 (SA), derived from the plant Arnebia nobilis, on normal and hydrocortisone-induced impaired healing in full thickness cutaneous punch wounds in rats. SA (0.1%) was applied topically daily as an ointment in polyethylene glycol base on wounds. SA treatment significantly accelerated healing of wounds, as measured by wound contraction compared to controls in hydrocortisone-impaired animals. SA treatment promoted formation of granulation tissue including cell migration and neovascularization, collagenization and reepithelialization. The expression of basic fibroblast growth factor (bFGF) was higher as revealed by immunohistochemistry in treated wounds compared to controls. However, the expression of transforming growth factor-β₁ was not affected by SA treatment. Since bFGF is known to accelerate wound healing, the increased expression of bFGF by SA may be partly responsible for the enhancement of wound healing. These studies suggest that SA could be further studied for clinical use to enhance wound healing.

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Picroliv preconditioning protects the rat liver against ischemia–reperfusion injury

Cited by 37 publications

References 34 publications

Erdosteine Improves Oxidative Damage in a Rat Model of Renal Ischemia-Reperfusion Injury

Erdosteine Improves Oxidative Damage in a Rat Model of Renal Ischemia-Reperfusion Injury

Fas Receptor Is Upregulated in Livers from Non-Heart-Beating Donors

Enhancement of Wound Healing by Shikonin Analogue 93/637 in Normal and Impaired Healing

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