Carrot is widely used as a foodstuff. The active components such as beta-carotene and panaxynol have been studied by many researchers. In this investigation of nonpolar active components from carrot, a new phenylpropanoid, epilaserine oxide ( 3), was isolated along with six known compounds, laserine ( 1), 2-epilaserine ( 2), panaxynol ( 4), ginsenoyne K ( 5), (8 E)-1,8-heptadecadiene-4,6-diyne-3,10-diol ( 6), and vaginatin ( 7). Their structures were deduced on the basis of spectroscopic methods. Significant cytotoxicity of 2-epilaserine against HL-60 cells was observed, which implied that phenylpropanoids were cytotoxic compounds in carrot. Laserine and 2-epilaserine in carrots from diverse locations in China were quantified by HPLC.

Panaxynol and panaxydol are naturally occurring polyacetylenes, isolated from the lipophilic fractions of Panax notoginseng, that exert anti-proliferative effects against malignant cells. However, to the best of our knowledge, no study concerning the inhibitory effects of the two polyacetylenes on cell growth of human promyelocytic leukemia cells has been reported. In this paper, we examined the antiproliferation and proapoptotic effects of panaxynol and panaxydol on HL60 cells and investigated their mechanism of action. Cell growth inhibition of panaxynol and panaxydol were determined by trypan blue dye exclusion assays. Apoptosis of cells was revealed by morphological observation, analysis for nuclear DNA distribution and by annexin V-FITC/ PI staining using flow cytometry. It was found that panaxynol and panaxydol markedly inhibited proliferation of HL60 cells in a time- and dose-dependent manner via an apoptotic pathway. In concern with these findings, Western blot analysis showed proteolytic activation of PKCδ, caspase-3 activation and cleavage of poly (ADP [adenosine diphosphate]-ribose) polymerase in HL60 cells treated by panaxynol and panaxydol. In conclusion, panaxynol and panaxydol have profound effects on growth and apoptosis of HL60 cells, suggesting those substances are worthy of further exploration as potential anti-cancer agents.

Mitochondrial function is critical in energy metabolism. To fully capture how the mitochondrial function changes in metabolic disorders, we investigated mitochondrial function in liver and muscle of animal models mimicking different types and stages of diabetes. Type 1 diabetic mice were induced by streptozotocin (STZ) injection. The db/db mice were used as type 2 diabetic model. High‐fat diet‐induced obese mice represented pre‐diabetic stage of type 2 diabetes. Oxidative phosphorylation (OXPHOS) of isolated mitochondria was measured with Clark‐type oxygen electrode. Both in early and late stages of type 1 diabetes, liver mitochondrial OXPHOS increased markedly with complex IV‐dependent OXPHOS being the most prominent. However, ATP, ADP and AMP contents in the tissue did not change. In pre‐diabetes and early stage of type 2 diabetes, liver mitochondrial complex I and II‐dependent OXPHOS increased greatly then declined to almost normal at late stage of type 2 diabetes, among which alteration of complex I‐dependent OXPHOS was the most significant. In contrast, muscle mitochondrial OXPHOS in HFD, early‐stage type 1 and 2 diabetic mice, did not change. In vitro, among inhibitors to each complex, only complex I inhibitor rotenone decreased glucose output in primary hepatocytes without cytotoxicity both in the absence and presence of oleic acid (OA). Rotenone affected cellular energy state and had no effects on cellular and mitochondrial reactive oxygen species production. Taken together, the mitochondrial OXPHOS of liver but not muscle increased in obesity and diabetes, and only complex I inhibition may ameliorate hyperglycaemia via lowering hepatic glucose production.

In this manuscript, chemical constituents, especially those with novel structures obtained from Acorus tatarinowii Schott (ATS), along with the pharmacological studies of those compounds, the volatile oil and the water soluble part of ATS, were reviewed.

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