Protective effect of Moutan Cortex extract on acetaminophen-induced hepatotoxicity in mice

Biological & Pharmaceutical Bulletin

Song

et al. 2017

Moutan Cortex, the root bark of Paeonia suffruticosa ANDREWS in Ranunculaceae, has widely demonstrated analgesic, anti-spasmodic, and anti-inflammatory effects in various cancer and immune cell lines. Oxidative stress is associated with development of several diseases, including liver disease. We prepared the water extract of Moutan Cortex (MCE) to investigate the cytoprotective activities and its mechanism. MCE protected hepatocytes from arachidonic acid (AA) iron induced oxidative stress, as indicated by reactive oxygen species (ROS) production and cell viability analysis. MCE also suppressed mitochondrial dysfunction in AA iron-treated human hepatocyte-derived hepatocellular carcinoma cell line, HepG2 cells. In addition, MCE treatment induces AMP-activated protein kinase (AMPK) and liver kinase B1 phosphorylation, which play a role in inhibition of oxidative stress induced cell death. Moreover, one of the MCE compounds, chlorogenic acid, exerted protective effects against oxidative stress and apoptosis. Taken together, MCE protected hepatocytes against AA iron-induced oxidative stress through AMPK activation, and may be a candidate for the treatment of liver disease.

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Moutan Cortex Protects Hepatocytes against Oxidative Injury through AMP-Activated Protein Kinase Pathway

Jang

Biological & Pharmaceutical Bulletin

Song

et al. 2017

“…For Mountan cortex radicis, there are no reports regarding its toxicity. Some reports have shown that Mountan cortex radicis has a protective effect on acute liver injury 8 and on acetaminophen-induced hepatotoxicity 9 . And there are many reports about the beneficial effect of paeonol, a major component of Mountan cortex radicis, such as anti-inflammatory effect 10 , protection of nephrotoxicity by Cisplatin 11 , and neuroprotective effect 12 .…”

Section: Discussionmentioning

confidence: 99%

Subchronic oral toxicity of herbal formula PM012 in Beagle dogs

Chung

et al. 2014

Mol. Cell. Toxicol.

PM012 is a modified oriental medicinal prescription based on Yukmijihwang-tang. We previously reported that PM012 has a neuro-protective effect and has no toxicity with chronic administration in rats. As a process of the development of herbal new drug, we assessed the oral toxicity of PM012 in Beagle dogs. PM012 was administered orally for 28 days at doses of 0, 250, 500, 1000 and 1500 mg/kg/day. When we analyzed the body weight gain, food consumption, clinical observations, blood biochemical, hematology, organ weight ratios and histopathological findings, there were no significant differences between the control and treated groups. It was concluded that orally administered PM012 was safe in dogs, and no treatment-related toxicity was detected, even at the highest doses investigated in repeated dose oral toxicity studies.

“…MCR has potent analgesic, sedative, anti-inflammatory, and anti-microbial properties (Jiang et al, 2007). Furthermore, MCR has a protective effect on acetaminophen-induced hepatotoxicity in mice (Shon and Nam, 2004). Paeonol, a major phenolic component of MCR, has recently been shown to alleviate alcoholic liver injury via inhibition of hepatic steatosis and inflammation (Hu et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Protective Effects of Moutan Cortex Radicis against Acute Hepatotoxicity

Park

Afr. J. Trad. Compl. Alt. Med.

Lee

2011

This study evaluated the potential beneficial effect of Moutan Cortex Radicis (MCR) in a murine model of carbon tetrachloride (CCl 4 )-, D-galactosamine (GalN)-and α-naphthylisothiocyanate (ANIT)-induced liver injury. Acute hepatotoxicity was induced by intraperitoneal injection of CCl 4 (10 μL/kg), GalN (700 mg/kg), and ANIT (40 mg/kg). Animals received MCR (30, 100, and 300 mg/kg ) orally at 48, 24, and 2 h before and 6 h after administration of CCl 4, GalN, and ANIT. Serum activities of aminotransferase were significantly higher at 24 h after CCl 4 or GalN treatment. These changes were attenuated by MCR. Histopathological analysis revealed multiple and extensive areas of portal inflammation, hepatocellular necrosis, and an increase in inflammatory cell infiltration. These changes were inhibited by MCR. Serum total bilirubin concentration increased and bile flow decreased significantly 48 h after ANIT treatment, which was attenuated by MCR. Our results suggest that MCR has a protective effect on acute liver injury.