Pim‐3 protects against hepatic failure in D‐galactosamine (D‐GalN)‐sensitized rats

Liu, L.-M.; Zhang, J.-X.; Wang, X.-P.; Guo, Hongxing; Deng, Huan; Luo, Jie

doi:10.1111/j.1365-2362.2009.02235.x

Cited by 16 publications

(19 citation statements)

References 41 publications

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“…In other words, the mechanism of the inhibitory effects, by which TQ protects against lipid peroxidation, may involve radical scavenging capability. Hepatotoxicity not only initiates lipid peroxidation but also reduces tissue GSH-px, GST, CAT, and SOD activities, and this depletion may result from oxidative modification of these proteins and our data are in line with other previous studies [32–36]. …”

Section: Discussionsupporting

confidence: 93%

Thymoquinone attenuates cisplatin-induced hepatotoxicity via nuclear factor kappa- β

Al-Malki

Sayed

2014

BMC Complement Altern Med

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BackgroundCisplatin (CP) is known as a potent anti-cancer drug. The most therapeutic adverse effect of CP is induced hepatotoxicity. In the present study, the protective effect of thymoquinone (TQ) on CP-induced hepatotoxicity was studied.MethodsWistar rats were divided into three groups (15 rats each). Group 1 served as the control group. Group 2 rats were injected ip with a single dose of CP (12 mg/kg b.w, i.p.). Group 3 rats were orally pre-treated with TQ (500 mg. kg−1. day−1) for one month, then the animals were injected i.p with CP 12 mg.kg−1.ResultsThe beneficial effects of TQ with its antioxidant/anti-inflammatory effects were observed. Injection of rats with CP markedly affected the liver functions and histopathological changes. The antioxidant enzyme activities and reduced glutathione (GSH) contents were significantly decreased while the levels of malondialdehyde (MDA) significantly increased. The electromobility shift assay (EMSA) showed a significant activation of NF-κB-p65 in the rat liver injected with CP. Furthermore, the expression and concentrations of inflammatory tumor necrosis factor (TNF-α), nitric oxide synthetase (iNOS), and interleukin (IL-1β) were markedly elevated in the CP injected rats. The administration of TQ improved all the altered functions, histopathology of the liver and attenuated the activated NF-κB. The antioxidant enzyme activities (glutathione peroxidase and glutathione –S transferase) of the rat livers were markedly increased while MDA was reduced as a result of TQ administration. In addition, the expression of TNF-α, iNOS, and IL-1β were markedly reduced.ConclusionIt was concluded that, TQ has potential benefits in the prevention of the onset and progression of CP induced hepatotoxicity.

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Section: Discussionsupporting

confidence: 93%

Thymoquinone attenuates cisplatin-induced hepatotoxicity via nuclear factor kappa- β

Al-Malki

Sayed

2014

BMC Complement Altern Med

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“…At 30 min after the injection, mice (NS, urantide) were challenged by an intraperitoneal injection with a total volume of 200 µl of NS (sham) or with 800 mg⋅kg −1 GalN and 50 µg⋅kg −1 LPS dissolved in 200 µl of NS as previously described [5] (LPS/GalN, urantide+LPS/GalN). Animal survival rates were calculated at 1, 2, 4, 6, 8, 12, 24 and 48 h after LPS/GalN injection, respectively.…”

Section: Methodsmentioning

confidence: 99%

“…As an animal model of ALF, lipopolysaccharide (LPS)/D-galactosamine (GalN)-challenged mice showed massive apoptosis in liver [4], [5]. Through crosstalking with innate immune system, the drugs can initiate the early immune injury of liver by stimulating production of proinflammatory cytokines [6].…”

Section: Introductionmentioning

confidence: 99%

Inhibition of UII/UTR System Relieves Acute Inflammation of Liver through Preventing Activation of NF-κB Pathway in ALF Mice

Dong

Liu

et al. 2013

PLoS ONE

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Urotensin II (UII) is implicated in immune inflammatory diseases through its specific high-affinity UT receptor (UTR). Enhanced expression of UII/UTR was recently demonstrated in the liver with acute liver failure (ALF). Here, we analysed the relationship between UII/UTR expression and ALF in lipopolysaccharide (LPS)/D-galactosamine (GalN)-challenged mice. Thereafter, we investigated the effects produced by the inhibition of UII/UTR system using urantide, a special antagonist of UTR, and the potential molecular mechanisms involved in ALF. Urantide was administered to mice treated with LPS/GalN. Expression of UII/UTR, releases of proinflammatory cytokines including tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β) and interferon-γ (IFN-γ), and activation of nuclear factor κB (NF-κB) signaling pathway were assessed in the lethal ALF with or without urantide pretreatment. We found that LPS/GalN-challenged mice showed high mortality and marked hepatic inflammatory infiltration and cell apoptosis as well as a significant increase of UII/UTR expression. Urantide pretreatment protected against the injury in liver following downregulation of UII/UTR expression. A close relationship between the acutely flamed hepatic injury and UII/UTR expression was observed. In addition, urantide prevented the increases of proinflammatory cytokines such as TNF-α, IL-1β and IFN-γ, and activation of NF-κB signaling pathway induced by LPS/GalN in mice. Thus, we conclude that UII/UTR system plays a role in LPS/GalN-induced ALF. Urantide has a protective effect on the acutely inflamed injury of liver in part through preventing releases of proinflammatory cytokines and activation of NF-κB pathway.

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“…The authors suggested that the SHANK3 gene product may play a role in autoimmunological response. The deleted region also includes the oncogene PIM3 which has previously been associated with liver disease in rats [Liu et al, 2010]. PIM3 encodes a serine/threonine protein kinase that is reported to be aberrantly expressed in human and mouse hepatitis but not normal liver.…”

mentioning

confidence: 99%

The 22q13.3 Deletion Syndrome (Phelan-McDermid Syndrome)

Phelan

McDermid²

2011

Mol Syndromol

394

320

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The 22q13.3 deletion syndrome, also known as Phelan-McDermid syndrome, is a contiguous gene disorder resulting from deletion of the distal long arm of chromosome 22. In addition to normal growth and a constellation of minor dysmorphic features, this syndrome is characterized by neurological deficits which include global developmental delay, moderate to severe intellectual impairment, absent or severely delayed speech, and neonatal hypotonia. In addition, more than 50% of patients show autism or autistic-like behavior, and therefore it can be classified as a syndromic form of autism spectrum disorders (ASD). The differential diagnosis includes Angelman syndrome, velocardiofacial syndrome, fragile X syndrome, and FG syndrome. Over 600 cases of 22q13.3 deletion syndrome have been documented. Most are terminal deletions of ∼100 kb to >9 Mb, resulting from simple deletions, ring chromosomes, and unbalanced translocations. Almost all of these deletions include the gene SHANK3 which encodes a scaffold protein in the postsynaptic densities of excitatory synapses, connecting membrane-bound receptors to the actin cytoskeleton. Two mouse knockout models and cell culture experiments show that SHANK3 is involved in the structure and function of synapses and support the hypothesis that the majority of 22q13.3 deletion syndrome neurological defects are due to haploinsufficiency of SHANK3, although other genes in the region may also play a role in the syndrome. The molecular connection to ASD suggests that potential future treatments may involve modulation of metabotropic glutamate receptors.

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Pim‐3 protects against hepatic failure in D‐galactosamine (D‐GalN)‐sensitized rats

Abstract: Pim-3 gene could protect rats from FHF by inhibiting liver apoptosis and improving inflammatory response of liver tissues, which could be associated with inhibiting expression of inflammatory mediators and promoting expression of anti-apoptosis protein Bcl-2.

Cited by 16 publications

References 41 publications

Thymoquinone attenuates cisplatin-induced hepatotoxicity via nuclear factor kappa- β

Thymoquinone attenuates cisplatin-induced hepatotoxicity via nuclear factor kappa- β

Inhibition of UII/UTR System Relieves Acute Inflammation of Liver through Preventing Activation of NF-κB Pathway in ALF Mice

The 22q13.3 Deletion Syndrome (Phelan-McDermid Syndrome)

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