Abstract
Leaf extract of Nelumbo nucifera (NLE) has been demonstrated to possess anti-atherosclerosis, improve alcohol-induced steatohepatitis, prevent high-fat diet-induced obesity, and inhibit the proliferation and metastasis of human breast cancer cells. This study determines the chemopreventive role of NLE against 2-acetylaminofluorene (AAF)-induced hepatocellular carcinoma (HCC) in rats. AAF was used to induce hepatocarcinogenesis in rats through genetic and nongenetic effects. After administration for 12 weeks, NLE (0.5–2%) supplementation orally inhibited AAF (0.03%)-induced hepatic fibrosis which appears during the development of premalignant lesions in rats. After the 6-month experiment, NLE supplementation resulted in decreasing AAF-induced serum parameters of hepatic injury, including the level of triglycerides, total cholesterol, alpha-fetoprotein (AFP), and inflammatory mediator interleukin (IL)-6 and tumor necrosis factor (TNF)-α as well as the activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma-glutamyl transferase (γGT). NLE supplementation also reduced AAF-induced lipid peroxidation and 8-hydroxy-2′-deoxyguanosine (8-OHdG) formation in the rat liver. Hepatic histopathological investigation revealed that NLE supplementation attenuated the AAF-induced HCC and glutathione S-transferase-Pi (GST-Pi) expression. Furthermore, NLE supplementation increased the expression of transcription factor, nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream targets, including catalase, glutathion peroxidase (GPx), and superoxide dismutase 1 (SOD-1) in the rat liver. Our findings indicate that NLE supplementation inhibited AAF-induced hepatocarcinogenesis by enhancing antioxidative potential and alleviating inflammation in rats.
Highlights
Hepatocellular carcinoma (HCC) is a common malignant tumor and has a high mortality rate worldwide
Six phenolic compounds were used as the standard, and the quantitative results revealed that nucifera leaf extract (NLE) contained compounds were used as the standard, and the quantitative results revealed that NLE contained gallic gallic acid (6.11 ± 0.15 μg/mg NLE), catechin (7.42 ± 0.69 μg/mg NLE), peltatoside (3.55 ± 0.04 μg/mg acid (6.11 ± 0.15 μg/mg NLE), catechin (7.42 ± 0.69 μg/mg NLE), peltatoside (3.55 ± 0.04 μg/mg NLE), NLE), rutin (4.65 ± 0.14 μg/mg NLE), isoquercitrin (2.83 ± 0.10 μg/mg NLE), miquelianin (8.81 ± 0.18 rutin (4.65 ± 0.14 μg/mg NLE), isoquercitrin (2.83 ± 0.10 μg/mg NLE), miquelianin (8.81 ± 0.18 μg/mg μg/mg NLE), and astragalin (0.75 ± 0.05 μg/mg NLE) through comparison of HPLC retention times
Our results demonstrated that NLE prevents AAF-induced hepatocarcinogenesis by increasing the expression and activity of the antioxidant enzymes and blocking reactive oxygen species (ROS) formation and inflammation (Figure 7)
Summary
Hepatocellular carcinoma (HCC) is a common malignant tumor and has a high mortality rate worldwide. 5-year survival rate of HCC is estimated to be below 20% [1]. The development of HCC is a complex process involving the accumulation of genetic and epigenetic alteration, which passes through states of initiation, promotion, and progression, with both viral and chemical carcinogens involved in the multistate process. The onset of HCC is usually late in patients with chronic liver diseases such as hepatitis B and C infections and dietary carcinogen exposure. Hepatic fibrosis occurs when liver is repeatedly and continuously injured. Untreated fibrosis may progress to liver cirrhosis, leading to organ failure and hepatoma [3,4]. Approaches on antioxidant, anti-inflammation, and anti-fibrosis are considered the effective strategy for lowering the morbidity and mortality of HCC
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