Abstract
Radiotherapy for treatment of hepatocellular carcinoma causes severe side effects, including acute hepatitis and chronic fibrosis. Complementary and alternative medicine (CAM) has emerged as an important part of integrative medicine in the management of diseases. Antrodia cinnamomea (AC), a valuable medicinal fungus originally found only in Taiwan, has been shown to possess anti-oxidation, vaso-relaxtation, anti-inflammation, anti-hepatitis, and anti-cancer effects. In this paper we evaluate the protective effects of ethanol extract of Antrodia cinnamomea (ACE) against radiotoxicity both in normal liver cell line CL48 and in tumor-bearing mice. In CL48, ACE protects cells by eliminating irradiation-induced reactive oxygen species (ROS) through the induction of Nrf2 and the downstream redox system enzymes. The protective effect of ACE was also demonstrated in tumor-bearing mice by alleviating irradiation-induced acute hepatitis. ACE could also protect mice from CCl4-induced hepatitis. Since both radiation and CCl4 cause free radicals, these results indicate that ACE likely contains active components that protect normal liver cells from free radical attack and can potentially benefit hepatocellular carcinoma (HCC) patients during radiotherapy.
Highlights
Radiation therapy remains an important regimen for the treatment of unresectable hepatocellular carcinoma (HCC)
The effect of Antrodia cinnamomea extract (ACE) treatment on cell survival was examined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay (Figure 1B)
Growth of CL48 cells was inhibited by irradiation (Figure 1A) or ACE (Figure 1B) in a dose-dependent manner
Summary
Radiation therapy remains an important regimen for the treatment of unresectable hepatocellular carcinoma (HCC). While radiotherapy is generally much more location specific and theoretically has fewer side effects than systemic chemotherapy, irradiation-induced hepatitis is still difficult to avoid. One of the important liver injuries due to irradiation is radiation-induced liver disease (RILD), or radiation hepatitis [1]. The primary effects of cellular exposure to ionizing radiation are direct destruction of DNA, lipids, and proteins, and indirect damage caused by the increased generation of reactive oxygen species (ROS) [3]. Increasing evidence demonstrates that the radiation-induced effects may be mediated through disruption of redox homeostasis and intercellular communications [6]. Radiation-mediated cleavage of water molecules can generate massive amounts of hydrogen peroxide and damage the mitochondrial respiratory chain to further produce excessive superoxide radicals [9]
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