Smad3 (Phospho-Ser213) ELISA Kit

Hepatocellular carcinoma (HCC) is one of the most prevalent malignancies, which ranks the third leading cause of cancer-related death worldwide. The screening of anti-HCC drug with high efficiency and low toxicity from traditional Chinese medicine (TCM) has attracted more and more attention. As a TCM, Chinese dragon's blood has been used for the treatment of cardiovascular illness, gynecological illness, skin disorder, otorhinolaryngological illness, and diabetes mellitus complications for many years. However, the anti-tumor effect and underlying mechanisms of Chinese dragon's blood remain ill-defined. Herein we have revealed that Chinese dragon's blood EtOAc extract (CDBEE) obviously suppressed the growth of human hepatoma HepG2 and SK-HEP-1 cells. Moreover, CDBEE inhibited the migration and invasion of HepG2 and SK-HEP-1 cells. Additionally, CDBEE displayed good in vitro anti-angiogenic activity. Importantly, CDBEE treatment significantly blunted the oncogenic capability of HepG2 cells in nude mice. Mechanistically, CDBEE inhibited Smad3 expression in human hepatoma cells and tumor tissues from nude mice. Using RNA interference, we demonstrated that CDBEE exerted anti-hepatoma activity partially through down-regulation of Smad3, one of major members in TGF-beta/Smad signaling pathway. Therefore, CDBEE may be a promising candidate drug for HCC treatment, especially for liver cancer with aberrant TGF-beta/Smad signaling pathway.

Purpose of review Pulmonary arterial hypertension (PAH) is characterized by pulmonary arterial endothelial cell (PAEC) dysfunction and apoptosis, pulmonary arterial smooth muscle cell (PASMC) proliferation, inflammation, vasoconstriction, and metabolic disturbances that include disrupted bone morphogenetic protein receptor (BMPR2)-peroxisome proliferator-activated receptor gamma (PPAR gamma) axis and DNA damage. Activation of PPAR gamma improves many of these mechanisms, although erroneous reports on potential adverse effects of thiazolidinedione (TZD)-class PPAR gamma agonists reduced their clinical use in the past decade. Here, we review recent findings in heart, lung, and kidney research related to the pathobiology of vascular remodeling and tissue fibrosis, and also potential therapeutic effects of the PPAR gamma agonist pioglitazone. Recent findings Independent of its metabolic effects (improved insulin sensitivity and fatty acid handling), PPAR gamma activation rescues BMPR2 dysfunction, inhibits TGF beta/Smad3/CTGF and TGF beta/pSTAT3/pFoxO1 pathways, and induces the PPAR gamma/apoE axis, inhibiting vascular remodeling. PPAR gamma activation dampens mtDNA damage via PPAR gamma/UBR5/ATM pathway, improves function of endothelial progenitor cells (EPCs), and decrease renal fibrosis by repressing TGF beta/pSTAT3 and TGF beta/EGR1. Pharmacological PPAR gamma activation improves many hallmarks of PAH, including dysfunction of BMPR2-PPAR gamma axis, PAEC, PASMC, EPC, mitochondria/metabolism, and inflammation. Recent randomized controlled trials, including IRIS (Insulin Resistance Intervention After Stroke Trial), emphasize the beneficial effects of PPAR gamma agonists in PAH patients, leading to recent revival for clinical use.