2012
DOI: 10.1016/j.jhep.2012.06.011
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Profound impact of gut homeostasis on chemically-induced pro-tumorigenic inflammation and hepatocarcinogenesis in rats

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Cited by 242 publications
(245 citation statements)
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References 36 publications
(36 reference statements)
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“…Among other antiangiogenic agents with less side effects, blockers of the reninangiotensin system such as angiotensin-I converting enzyme inhibitor and angiotensin-II type 1 blocker have been proved to be promising adjunctive to HCC therapy showing synergistic effects in inhibiting hepatocarcinogenesis (15). Like other two probiotics (8,9), Prohep is now expected to suppress the tumor growth in an orthotopic model. Our concern is not only its effect on angiogenesis and carcinogenesis but also its interactions with other key mediators and various constituent cells in the liver.…”
Section: Authors Next Found That the Proportion Of Th17 Cells In Totamentioning
confidence: 99%
“…Among other antiangiogenic agents with less side effects, blockers of the reninangiotensin system such as angiotensin-I converting enzyme inhibitor and angiotensin-II type 1 blocker have been proved to be promising adjunctive to HCC therapy showing synergistic effects in inhibiting hepatocarcinogenesis (15). Like other two probiotics (8,9), Prohep is now expected to suppress the tumor growth in an orthotopic model. Our concern is not only its effect on angiogenesis and carcinogenesis but also its interactions with other key mediators and various constituent cells in the liver.…”
Section: Authors Next Found That the Proportion Of Th17 Cells In Totamentioning
confidence: 99%
“…The results showed that translocation of gut organisms to mesenteric lymph nodes was increased in patients with advanced cirrhosis and was reduced to the level found in non-cirrhotic patients by selective intestinal decontamination. There was also evidence showing that gut microbiota might promote liver fibrosis in mice, and the increase in bacterial translocation from gut to liver was associated with chemically induced fibrosis [19]. …”
Section: Roles Of Gut Microbiota In Hepatocarcinogenesismentioning
confidence: 99%
“…Thus, enhanced intestinal permeability to endotoxins appears to be the primary cause of chemically induced endotoxemia. This finding was supported by the fact that reduction of LPS using antibiotics in rats or genetic ablation of its receptor TLR4 in mice dramatically mitigated enteric dysbiosis, decreased liver tumor growth and prevented tumor multiplicity [19]. Yu et al [39] suggested that reducing gut injury, improving blood flow to the gastrointestinal tract and lessening the gut translocation of endotoxin might improve liver function.…”
Section: Roles Of Gut Microbiota In Hepatocarcinogenesismentioning
confidence: 99%
“…20 In rat models of hepatocarcinogenesis, induction of gut dysbiosis significantly promoted carcinogenesis. 21 Another report indicates that microbiota may not be involved in initiation of hepatocellular carcinoma but in promotion and proliferation of hepatocellular carcinoma. 22 Changes in microbiota have also been implicated in causation of hepatic encephalopathy, but the reports are conflicting.…”
Section: Microbiota and Liver Diseasementioning
confidence: 99%