huvecs

Dopamine hydrochloride (ASL279), a naturally occurring catecholamine formed by decarboxylation of dihydroxyphenylalanine and a precursor of norepinephrine and epinephrine, binds to alpha-1- and beta-1- adrenergic receptors.

3-Hydroxybenzaldehyde is a compound useful in organic synthesis.

L-Cystathionine dihydrochloride is a non-protein sulfur-containing compound that plays a critical role in the metabolism of sulfur-containing amino acids (amino acids). It helps prevent homocysteine-induced, mitochondria-dependent apoptosis (apoptosis) in human umbilical vein endothelial cells (HUVECs) and is important in cardiovascular protection.

1. Acetylshikonin exhibits weak cytotoxicity against human umbilical vein endothelial cells (HUVECs) with IC5 of over 2 microM, exhibits the antiangiogenic and antitumorigenic effects by suppressing proliferation and angiogenic factors. 2. Acetylshikonin inhibits the generation of NADPH oxidase complex in the activation of respiratory burst of PMNs, but does not directly inhibit the activity of NADPH oxidase already generated. 3. Certain shikonin derivatives(such as Acetylshikonin) act as modulators of the Nur77-mediated apoptotic pathway and identify a new shikonin-based lead that targets Nur77 for apoptosis induction. 4. Acetylshikonin, shikonin, and alkannin have accelerative effect on the proliferation of granulation tissue in rats. 5. Acetylshikonin has inhibitory effect on the edematous response is due neither to the release of steroid hormones from the adrenal gland nor to the glucocorticoid activity, but probably partly to the suppression of mast cell degranulation and partly to protection of the vasculature from mediator challenge. 6. Acetylshikonin induces apoptosis of hepatitis B virus X protein-expressing human hepatocellular carcinoma cells via endoplasmic reticulum stress.

Aureothricin, a dithiolopyrrolone (DTP) antibiotic originally derived from Streptomyces, demonstrates a broad-spectrum of antibacterial effectiveness. Additionally, it inhibits the adhesion of human umbilical vein endothelial cells (HUVECs) to vitronectin[1].

Cyanidin-3-O-arabinoside chloride has antioxidant activity. It reduces the peroxynitrite-induced suppression of mitochondrial respiration, DNA damage, PARS activation and vascular dysfunction in HUVECs.

Jolkinolide A has anti-tumor activity. It inhibited VEGF expression in A549 cells through the inhibition of the Akt-STAT3-mTOR signaling pathway, and directly inhibited the proliferation and migration of HUVECs.

Pyranonigrin A is a fungal metabolite originally isolated from Aspergillus that has antioxidant activity. It scavenges 2,2-diphenyl-1-picrylhydrazyl (DPPH;) free radicals in a cell-free assay (IC50 = 132.9 μM). Pyranonigrin A (10 μM) suppresses TNF-α-induced expression of vascular cell adhesion molecule 1 (VCAM-1) in human umbilical vein endothelial cells (HUVECs).

(+)-Macrosphelide A is a fungal metabolite originally isolated from Microsphaeropsis. It inhibits adhesion of HL-60 human leukemia cells to human umbilical vein endothelial cells (HUVECs) in a concentration-dependent manner. It also inhibits the growth of SKOV3 ovarian cancer cells in a concentration-dependent manner. (+)-Macrosphelide A inhibits the growth of Gram-positive bacteria, including B. subtilis, M. luteus, B. thuringiensis, and S. aureus (MICs = 143, 143, 57, and 57 μg/ml, respectively), but not Gram-negative bacteria or fungi.

Epifriedelanol (Epifriedelinol) suppresses adriamycin-induced cellular senescence, replicative senescence in human fibroblasts (HDFs) and HUVECs. Because of Epifriedelanol can reduce cellular senescence in human primary cells, it may be used to develop dietary supplements or cosmetics that modulate tissue aging or aging-associated diseases.