Modulation of the inflammatory response and apoptosis using epidermal growth factor and hepatocyte growth factor in a liver injury model: a potential approach to the management and treatment of cholestatic liver disease

Thatch, Keith A.; Schwartz, Marshall Z.; Yoo, Edward Y.; Mendelson, Kim G.; Duke, Duane S.

doi:10.1016/j.jpedsurg.2008.08.045

Cited by 15 publications

(16 citation statements)

References 25 publications

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“…The HGF supplementation group received 250 μg kg −1 d −1 of recombinant human HGF (Genentech, San Francisco, CA). This concentration is consistent with the optimal dosage determined in previous in vivo studies for enhancement of bowel function and modulation of liver function [8,10,11].…”

Section: Experimental Modelsupporting

confidence: 90%

“…Our recent research demonstrated that HGF modulates the hepatic inflammatory response, downregulates apoptosis, and promotes hepatic regeneration in response to a single cholestatic insult [8]. Previous studies have also demonstrated the ability of HGF to decrease cholestasis and improve the hepatic regenerative process [33].…”

Section: Discussionmentioning

confidence: 96%

“…Recently, we have focused on potential roles of growth factors in modulating the hepatic inflammatory response to liver injury. Our initial research demonstrated that after a single injection of the cholestatic agent α-naphtylisocyocyanate (ANIT), hepatocyte growth factor (HGF) and epidermal growth factor supplementation improves the hepatic inflammatory response [8]. However, the injury to the liver by TPN causes progressive intrahepatic cholestasis, hepatic steatosis, portal tract fibrosis and infiltration, and ultimately hepatic failure [6,9].…”

mentioning

confidence: 99%

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Growth factor modulation of hepatic inflammation: a novel approach to the management of total parenteral nutrition–associated liver disease

Thatch

Katz

Haber

et al. 2010

Journal of Pediatric Surgery

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Section: Experimental Modelsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 96%

mentioning

confidence: 99%

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Growth factor modulation of hepatic inflammation: a novel approach to the management of total parenteral nutrition–associated liver disease

Thatch

Katz

Haber

et al. 2010

Journal of Pediatric Surgery

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“…Previous reports have demonstrated that bile acid synthesis may be inhibited during liver damage [33,34] . The present study demonstrated that sweroside significantly attenuated the down-regulation of Cyp7a1, Cyp8b1, and Hsd3b7, which is consistent with results from previous reports [14,17] .…”

Section: Discussionmentioning

confidence: 97%

“…The upregulation of Oatp1a1 by sweroside treatment in the present study is consistent with the reduction of TCA and TDCA in the liver. The modulation of pro-inflammatory responses plays a critical role in cholestatic liver injury [33] . The present study demonstrated that hepatic MPO activity was significantly increased after ANIT exposure, which is consistent with results from a previous study [34] .…”

Section: Discussionmentioning

confidence: 99%

Sweroside ameliorates α-naphthylisothiocyanate-induced cholestatic liver injury in mice by regulating bile acids and suppressing pro-inflammatory responses

Yang

Gong

et al. 2016

Acta Pharmacol Sin

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Aim: Sweroside is an iridoid glycoside with diverse biological activities. In the present study we investigated the effects of sweroside on α-naphthylisothiocyanate (ANIT)-induced cholestatic liver injury in mice. Methods: Mice received sweroside (120 mg·kg -1 ·d -1 , ig) or a positive control INT-747 (12 mg·kg -1 ·d -1 , ig) for 5 d, and ANIT (75 mg/kg, ig) was administered on d 3. The mice were euthanized on d 5, and serum biochemical markers, hepatic bile acids and histological changes were analyzed. Hepatic expression of genes related to pro-inflammatory mediators and bile acid metabolism was also assessed. Primary mouse hepatocytes were exposed to a reconstituted mixture of hepatic bile acids, which were markedly elevated in the ANIT-treated mice, and the cell viability and expression of genes related to pro-inflammatory mediators were examined. Results: Administration of sweroside or INT-747 effectively ameliorated ANIT-induced cholestatic liver injury in mice, as evidenced by significantly reduced serum biochemical markers and attenuated pathological changes in liver tissues. Furthermore, administration of sweroside or INT-747 significantly decreased ANIT-induced elevation of individual hepatic bile acids, such as β-MCA, CA, and TCA, which were related to its effects on the expression of genes responsible for bile acid synthesis and transport as well as pro-inflammatory responses. Treatment of mouse hepatocytes with the reconstituted bile acid mixture induced significant pro-inflammatory responses without affecting the cell viability. Conclusion: Sweroside attenuates ANIT-induced cholestatic liver injury in mice by restoring bile acid synthesis and transport to their normal levels, as well as suppressing pro-inflammatory responses.

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Proteomic analysis of plasma from rats following total parenteral nutrition‐induced liver injury

et al. 2015

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Total parenteral nutrition (TPN) is provided as the primary nitrogen source to manage patients with intestinal failure who were not able to sustain themselves on enteral feeds. The most common complication of long-term TPN use is hepatitis. A proteomic approach was used to identify proteins that are differentially expressed in the plasma of rats following TPN-related acute liver injury. Six male rats were randomly assigned to either the saline infusion control group or the TPN infusion group. Our results demonstrate that TPN infusion in rats resulted in hepatic dysfunction and hepatocyte apoptosis. Five proteins that were differentially expressed between TPN infusion and normal rats were determined and validated in vivo. Fascinatingly, the proteomic differential displays, downregulated proteins included peroxiredoxin 2 (PRDX2), alpha-1-antiproteinase (A1AT), and fibrinogen gamma chain (FIBG), which were involved in oxidative stress, inflammatory respondence and cells apoptosis. After TPN infusion, two protein spots showed increased expression, namely, the glucagon receptor (GLR) protein and apolipoprotein A-1 (APOA1), which may mediate the effects of TPN administration on glycogen and lipid metabolism. In this study, proteomic analysis suggested TPN-related acute liver injury could be involved in limiting cellular protection mechanisms against oxidative stress-induced apoptosis. On the basis of the results, we also give molecular evidences replying TPN-related hepatitis.

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Modulation of the inflammatory response and apoptosis using epidermal growth factor and hepatocyte growth factor in a liver injury model: a potential approach to the management and treatment of cholestatic liver disease

Cited by 15 publications

References 25 publications

Growth factor modulation of hepatic inflammation: a novel approach to the management of total parenteral nutrition–associated liver disease

Growth factor modulation of hepatic inflammation: a novel approach to the management of total parenteral nutrition–associated liver disease

Sweroside ameliorates α-naphthylisothiocyanate-induced cholestatic liver injury in mice by regulating bile acids and suppressing pro-inflammatory responses

Proteomic analysis of plasma from rats following total parenteral nutrition‐induced liver injury

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