Chlorella is a green unicellular alga that is commercially produced and distributed worldwide as a dietary supplement. Chlorella products contain numerous nutrients and vitamins, including D and B12, that are absent in plant-derived food sources. Chlorella contains larger amounts of folate and iron than other plant-derived foods. Chlorella supplementation to mammals, including humans, has been reported to exhibit various pharmacological activities, including immunomodulatory, antioxidant, antidiabetic, antihypertensive, and antihyperlipidemic activities. Meta-analysis on the effects of Chlorella supplementation on cardiovascular risk factors have suggested that it improves total cholesterol levels, low-density lipoprotein cholesterol levels, systolic blood pressure, diastolic blood pressure, and fasting blood glucose levels but not triglycerides and high-density lipoprotein cholesterol levels. These beneficial effects of Chlorella might be due to synergism between multiple nutrient and antioxidant compounds. However, information regarding the bioactive compounds in Chlorella is limited.

Acanthopanax senticosus (Rupr. et Maxim) Harms (ASH), also known as Siberian ginseng or eleuthero, is a hardy shrub native to China, Korea, Russia and the northern region of Japan. ASH is used for the treatment of several diseases such as heart disease, hypertension, rheumatoid arthritis, allergies, chronic bronchitis, diabetes and cancer. In the present study, the inhibitory effect of the root extract of ASH (ASHE) on HuH-7 and HepG2 liver cancer cells was examined. ASHE suppressed liver cancer cell proliferation by inducing cell cycle arrest at the G0/G1 phase, as well as apoptosis, as indicated by the increased number of Annexin V and 7-AAD-positive cells. Furthermore, the expression of LC3-II, an autophagy marker, in these cells also increased post treatment with ASHE. LC3-II induction was further enhanced by co-treatment with chloroquine. Fluorescence and transmission electron micrographs of ASHE-treated liver cancer cells showed the presence of an increased number of autophagic vesicles. A decreased protein expression level of run domain Beclin-1-interacting and cysteine-rich domain-containing, an autophagy inhibitor, with no change in RUBCN mRNA expression was observed, indicating activation of the autophagosome-lysosome fusion step of autophagy. In conclusion, ASHE exerts cytostatic activity on liver cancer cells via both apoptosis and autophagy, and may serve as a potential therapeutic agent for management of liver cancer and autophagy-related diseases.

This study examined the effects of oral administration of water extract of chlorella (WEC) (100 mg/kg bodyweight) and phenethylamine (10 μg/kg bodyweight) on high-fat diet (HFD)-induced liver damage in mice. Phenethylamine significantly mitigated HFD-induced lipid oxidation (generation of malondialdehyde) and liver damage without markedly decreasing hepatic lipid accumulation. WEC exerted similar effects although with decreased efficacy. In addition, WEC and phenethylamine decreased the methylglyoxal levels and increased the glyceraldehyde 3-phosphate dehydrogenase (GAPDH) protein levels in the liver. Methylglyoxal is generated from substrates of GAPDH, dihydroxyacetone phosphate and glyceraldehyde 3-phosphate. These facts indicate that methylglyoxal triggers oxidation of accumulated lipid, which generates malondialdehyde and consequently induces liver damage. Suppression of generation of toxic aldehydes by WEC and phenethylamine was also confirmed by maintaining hepatic cysteine, highly reactive to aldehydes. Thus, trace amounts of phenethylamine alleviate HFD-induced liver damage by regulating methylglyoxal via increase of GAPDH.

Hot water extract of chlorella (WEC) increased the lifespan of superoxide dismutase (SOD)-1 mutant adults of Drosophila melanogaster in a dose dependent manner (200–800 µg/mL). Compounds in WEC were successively fractionated by solid phase extraction using a Sep-Pak C18 cartridge and size exclusion chromatography (SEC). Amino compounds in SEC fractions were derivatized with 6-aminoquinolyl-N-hydroxylsuccinimidyl carbamate and analyzed by reversed phased-liquid chromatography-tandem mass spectrometry. Phenylalanine, phenethylamine, isopentylamine, and 2-methylbutylamine were identified in the SEC fraction, which increased the lifespan of the D. melanogaster mutant adults. Phenethylamine, at very low doses (6–60 ng/g of diet) that roughly corresponded to those of phenethylamine in WEC (200–800 μg/mL), increased the lifespan of the D. melanogaster adults, while isopentylamine did not exert the lifespan elongation activity. Since phenethylamine did not show SOD-like activity, it did not increase lifespan by direct antioxidant activity.

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