The fruit of Acanthopanax senticosus Harms improves arterial stiffness and blood pressure: a randomized, placebo-controlled trial.

BACKGROUND/OBJECTIVES: Arterial stiffness and endothelial dysfunction are 2 of the independent predictors for cardiovascular disease, while Acanthopanax senticosus Harms (ASH) is a traditional medicinal plant that can improve cardiovascular health. This study aimed to investigate the efficacy of the fruit of ASH on vascular function in apparently healthy subjects. SUBJECTS/METHODS: A 12-week, randomized, double-blind, placebo-controlled design, consisting of healthy adults with at least 2 of the following 3 conditions: borderline high blood pressure (BP; 120 mmHg ≤ systolic BP ≤ 160 mmHg or 80 mmHg ≤ diastolic BP ≤ 100 mmHg), smoking (≥10 cigarettes/day), and borderline blood lipid levels (220 ≤ total cholesterol ≤ 240, 130 ≤ low density lipoprotein cholesterol ≤ 165, or 150 ≤ triglyceride ≤ 220 mg/dL). Randomly assigned 76 subjects who received a placebo or 2 doses of ASH fruit (low, 500 mg/day; high, 1,000 mg/day) completed the intervention. Brachial-ankle pulse wave velocity (baPWV), flow-mediated dilation, carotid intima-media thickness, and BP were measured both at baseline and following the 12-week intervention. Endothelial nitric oxide synthase (eNOS) phosphorylation was assessed by western blotting. RESULTS: Compared with the placebo group, the low-dose group showed more significant changes after the 12-week intervention period in terms of systolic BP (0.1 vs. -7.7 mmHg; P = 0.044), baPWV (31.3 vs. -98.7 cm/s; P = 0.007), and the ratio of phospho-eNOS/eNOS (0.8 vs. 1.22; P = 0.037). CONCLUSIONS: These results suggest that ASH fruit extract at 500 mg/day has the potential to improve BP and arterial stiffness via endothelial eNOS activation in healthy adults with smoking and the tendency of having elevated BP or blood lipid parameters. TRIAL REGISTRATION: Clinical Research Information Service Identifier: KCT0001072.

Peroxidase and photoprotective activities of magnesium protoporphyrin IX.

Magnesium-protoporphyrin IX (Mg-PPn), which is formed through chelation of protoporphyrin IX (PPn) with Mg ion by Mg chelatase, is the first intermediate for the (bacterio)chlorophyll biosynthetic pathway. Interestingly, Mg-PPn provides peroxidase activity (approximately 4 × 10(-2) units/micrometer) detoxifying H2O2 in the presence of electron donor(s). The peroxidase activity was not detected unless PPn was chelated with Mg ion. Mg-PPn was found freely diffusible through the membrane of Escherichia coli and Vibrio vulnificus, protecting the cells from H2O2. Furthermore, unlike photosensitizers such as tetracycline and PPn, Mg-PPn did not show any phototoxicity, but rather it protected cell from ultraviolet (UV)-A-induced stress. Thus, the exogenous Mg-PPn could be used as an antioxidant and a UV block to protect cells from H2O2 stress and UV-induced damage.

Crude saponins from Platycodon grandiflorum induce apoptotic cell death in RC-58T/h/SA#4 prostate cancer cells through the activation of caspase cascades and apoptosis-inducing factor.

Saponins are a major active component of Platycodon grandiflorum (P. grandiflorum) and are known to induce apoptosis in metastatic prostate cancer cell lines. However, thus far, no research has been conducted on the anticancer activity of saponins in RC-58T/h/SA#4 primary prostate cancer cells. In this study, we show that the treatment of prostate cancer cells with saponins extracted from P. grandiflorum (SPG) inhibits cell proliferation in a dose-dependent manner. SPG significantly induced apoptotic cell death, resulting in an increase in the sub-G1 apoptotic cell population, apoptotic DNA fragmentation and morphological changes. Pre-treatment with a caspase inhibitor modestly attenuated the SPG-induced increase in the sub-G1 cell population, suggesting that caspases play a role in SPG-induced apoptosis. Moreover, SPG-induced apoptosis was associated with changes in caspase activity, the upregulation of the apoptotic protein, Bax and the downregulation of the anti-apoptotic protein, Bcl-2. Furthermore, the caspase-independent mitochondrial apoptosis factor, apoptosis-inducing factor (AIF) was upregulated following SPG treatment. These findings indicate that SPG exerts its anticancer effects on RC-58T/h/SA#4 primary prostate cancer cells through mitochondrial caspase-dependent and -independent apoptotic pathways.