Effects of Sho-saiko-to on hepatocarcinogenesis and 8-hydroxy-2'-deoxyguanosine formation

Shiota, Goshi; Maeta, Yoshiko; Mukoyama, Tomoyuki; Yanagidani, Atsushi; Udagawa, Akihide; Oyama, Kenji; Yashima, Kazuo; Kishimoto, Yosuke; Nakai, Yoichiro; Miura, Tetsuo; Ito, Hisao; Murawaki, Yoshikazu; Kawasaki, Hironaka

doi:10.1053/jhep.2002.33066

Cited by 64 publications

(52 citation statements)

References 28 publications

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“…Our findings suggested that HCV related HCC does not exclusively employ steatosis as a precondition; rather, HCV only acts as a "second hit" on the backdrop of chemically induced genetic injury. Given data that DEN can generate reactive oxygen species (ROS) and enhance oxidative stress, [16][17][18][19] it is tempting to speculate that DEN and steatosis, another known cause of ROS, may act in similar manners to predispose hepatocytes to genotoxic injury and malignant transformation.…”

Section: Discussionmentioning

confidence: 99%

Hepatitis C virus acts as a tumor accelerator by blocking apoptosis in a mouse model of hepatocarcinogenesis†

et al. 2005

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We developed hepatitis C virus (HCV) core-E1-E2 and HCV core transgenic mice on a common genetic background to assess the contribution of HCV structural proteins to hepatocarcinogenesis. Eight-week-old core-E1-E2, core, and nontransgenic mice inbred on the FVB؋C57Bl/6 background were treated with diethylnitrosamine (DEN) and sacrificed at 32 weeks old. Proliferation and apoptosis were assessed by immunohistochemistry. H epatitis C virus (HCV) infects an estimated 170 million people worldwide, and 2.7 million people in the United States harbor active HCV infection. 1 Chronic HCV infection has been independently established as a leading cause of hepatocellular carcinoma (HCC). Unlike hepatitis B virus (HBV), the RNA genome of HCV does not integrate into the host chromosome. HCV-related hepatocarcinogenesis is, therefore, not likely to involve insertional mutagenesis. Rather, it has been hypothesized that HCV produces HCC through the cumulative effects of chronic infection, injury and repair. Whether HCV proteins are directly oncogenic has not been established. Unfortunately, the lack of an appropriate small animal model of HCV has impeded progress in defining the molecular mechanisms of HCV-induced carcinogenesis.We originally developed an HCV transgenic mouse model encoding the core, E1, and E2 structural proteins under the control of the albumin promoter on the FVB background; despite high-level protein expression, this model did not develop hepatic pathology. 2 However, more recently, Moriya et al. developed a transgenic mouse model on the C57Bl/6 background that overexpresses Abbreviations: HCV, hepatitis C virus; DEN, diethylnitrosamine; HCC, hepatocellular carcinoma; AI, apoptotic index; PI, proliferation index. From the

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Section: Discussionmentioning

confidence: 99%

Hepatitis C virus acts as a tumor accelerator by blocking apoptosis in a mouse model of hepatocarcinogenesis†

et al. 2005

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“…A later prospective, randomized (albeit nonblind) study by Oka et al [410] could elucidate the use of TJ-9 in preventing the development of HCC in patients with cirrhosis, particularly in patients without HBsAg. Successive studies continued to confirm that TJ-9 could protect experimental liver injury caused by D-galactosamine and liver fibrosis by inhibition of lipid peroxide formation in liver cells [411,412].…”

Section: Tertiary Prevention Of Hcv-related Hccmentioning

confidence: 96%

Asian Pacific Association for the Study of the Liver consensus recommendations on hepatocellular carcinoma

et al. 2010

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Introduction The Asian Pacific Association for the Study of the Liver (APASL) convened an international working party on the management of hepatocellular carcinoma (HCC) in December 2008 to develop consensus recommendations. Methods The working party consisted of expert hepatologist, hepatobiliary surgeon, radiologist, and oncologist from Asian-Pacific region, who were requested to make drafts prior to the consensus meeting held at Bali, Indonesia on 4 December 2008. The quality of existing evidence and strength of recommendations were ranked from 1 (highest) to 5 (lowest) and from A (strongest) to D (weakest), respectively, according to the Oxford system of evidence-based approach for developing the consensus statements. 123Hepatol Int (2010) 4: 439-474 DOI 10.1007/s12072-010-9165-7 Results Participants of the consensus meeting assessed the quality of cited studies and assigned grades to the recommendation statements. Finalized recommendations were presented at the fourth APASL single topic conference on viral-related HCC at Bali, Indonesia and approved by the participants of the conference.

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“…Although the mechanism by which Sho-saiko-to protects hepatocytes against liver disease is not fully elucidated, clinical trials have shown its efficacy in patients with chronic hepatitis and liver cirrhosis in Japan, Korea and China. Some plausible actions as an antioxidant have been reported, for example, scavenging free radicals [60,61] and reducing the hepatic level of malondialdehyde, a product of lipid peroxidation [62] . Shiota et al [61] demonstrated that TJ-9 lowered diethylnitrosamine-induced ROS, resulting in reduction of 8-OHdG formation and hepatocarcinogenesis in rats.…”

Section: Sho-saiko-to (Tj-9 Xiao-chai-hu-tang)mentioning

confidence: 99%

“…Some plausible actions as an antioxidant have been reported, for example, scavenging free radicals [60,61] and reducing the hepatic level of malondialdehyde, a product of lipid peroxidation [62] . Shiota et al [61] demonstrated that TJ-9 lowered diethylnitrosamine-induced ROS, resulting in reduction of 8-OHdG formation and hepatocarcinogenesis in rats. A double-blind multicenter trial reported an improvement in AST and ALT values in 116 chronic hepatitis patients treated with TJ-9 for 12 wk [63] .…”

Section: Sho-saiko-to (Tj-9 Xiao-chai-hu-tang)mentioning

confidence: 99%

Prevention of hepatocellular carcinoma: Focusing on antioxidant therapy

Miyanishi

Hoki

Tanaka

et al. 2015

WJH

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Oxidative stress has been investigated in the context of alcoholic liver injury for many years and shown to be a causal factor of chronic hepatitis C (CHC), nonalcoholic steatohepatitis (NASH), drug-induced liver injury, Wilson' s disease, and hemochromatosis. In CHC, it has been demonstrated that oxidative stress plays an important role in hepatocarcinogenesis. In cases with persistent hepatitis due to failure of hepatitis C virus eradication, or chronic liver disease, such as NASH, the treatment of which remains unestablished, it is important to reduce serum alanine aminotransferase levels and prevent liver fibrosis and development of hepatocellular carcinoma. This also suggests the importance of antioxidant therapy. Among treatment options where it would be expected that anti-inflammatory activity plays a role in their confirmed efficacy for chronic hepatitis, iron depletion therapy, glycyrrhizin, ursodeoxycholic acid, Sho-Saiko-To, and vitamin E can all be considered antioxidant therapies. To date, however, the ability of these treatments to prevent cancer has been confirmed only in CHC. Nevertheless, anti-inflammatory and antifibrotic effects have been demonstrated in other liver diseases and these therapies may potentially be effective for cancer prevention.

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Effects of Sho-saiko-to on hepatocarcinogenesis and 8-hydroxy-2'-deoxyguanosine formation

Cited by 64 publications

References 28 publications

Hepatitis C virus acts as a tumor accelerator by blocking apoptosis in a mouse model of hepatocarcinogenesis†

Hepatitis C virus acts as a tumor accelerator by blocking apoptosis in a mouse model of hepatocarcinogenesis†

Asian Pacific Association for the Study of the Liver consensus recommendations on hepatocellular carcinoma

Prevention of hepatocellular carcinoma: Focusing on antioxidant therapy

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