No abstract

Carthamus tinctorius L., known as safflower, has been used in traditional treatment for cardiovascular, cerebrovascular, and diabetic vascular complications. We proposed to investigate how the ethanol extract of Carthamus tinctorius L. (ECT) can be used ethnopharmacologically and alleviate vascular inflammatory processes under cytokine stimulation in human vascular endothelial cells. Using the optimized HPLC method, six markers were simultaneously analyzed for quality control of ECT. Pretreatment with ECT (10–100 μg/mL) significantly reduced the increase of leukocyte adhesion to HUVEC by TNF-α in a dose-dependent manner. Cell adhesion molecules (CAMs) such as intracellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and endothelial cell selectin (E-selectin) are decreased by ECT. In addition, ECT significantly suppressed TNF-α-induced oxidative stress referring to reactive oxygen species (ROS) production. p65 NF-κB nuclear translocation and its activation were inhibited by ECT. Furthermore, pretreatment of ECT increased the HO-1 expression, and nuclear translocation of Nrf-2. These data suggest the potential role of ECT as a beneficial therapeutic herb in vascular inflammation via ROS/NF-kB pathway and the regulation of Nrf-2/HO-1 signaling axis is involved in its vascular protection. Thus, further study will be needed to clarify which compound is dominant for protection of vascular diseases.

Cardiac hypertrophy is characterized by increased cardiomyocyte size including physiological and pathological hypertrophy. Doxorubicin (DOX) widely used as the most potent anthracycline antibiotic agents for a wide range of cancers. DOX is induce cardiac hypertrophy because of it has a dose‐limiting side effect such as dilated cardiomyopathy and lipid peroxidation. TongGuanWan (TGW, 通關丸), a well‐known traditional herbal formula, has been reported that delay atherosclerotic formation and development and improving diabetes. which is most closely related to diabetes mellitus. However, the protective effect of TGW on cardiac hypertrophy and fibrosis was not investigated. The aim of this study was to investigate the effects of TGW on cardiac hypertrophy and fibrosis, which has been implicated in heart failure in H9c2 cells and isoproterenol (ISO)‐induced cardiac hypertrophy mice. In vitro, H9c2 cells were induced by DOX (1 μM) in the presence or absence of TGW (1–10 μg/ml) and incubated for 24 h. In vivo, TGW was administrated to ISO‐induced cardiac hypertrophy mice (n=8) to 100 and 200 mg/kg/day concentrations, respectively. The experiment was measured for 2 weeks following TGW respectively. The results of in vitro study indicated that TGW inhibit the increase cell surface area and the upregulation of hypertrophy markers including atrial natriuretic peptide (ANP), B‐type natriuretic peptide (BNP), beta‐myosin heavy chain (β‐MHC), and Myosin Light Chain‐2 (MLC2) in H9c2 cells. In addition, TGW reduced DOX‐induced the MAPKs protein expression and NF‐κB p65 activation in H9c2 cells. TGW treatment remarkably inhibit activation of GATA‐4/calcineurin/NFAT‐3 signaling pathway under DOX conditions. Moreover, TGW significantly reduce DOX‐induced expression of cell apoptosis‐related proteins and fibrosis biomarkers. The results of in vivo study indicated that TGW significantly reduced the heart weight mass to body weight ratio (HW/BW) and left ventricle mass to body weight ratio (LV/BW) levels compared to the untreated the ISO‐induced cardiac hypertrophy mice. Administration of TGW reduced protein expression of hypertrophy markers in cardiac hypertrophy mice. Moreover, TGW showed decreased that perivascular fibrosis and vessel hypertrophy in the heart tissues of cardiac hypertrophy mice, as determined by Picro‐Sirius Red staining. TGW group significantly inhibited protein and mRNA expression levels of fibrosis related factors such as fibronectin, α‐SMA and collagen type I compared to the untreated the ISO‐induced cardiac hypertrophy group. Therefore, these results suggest that TGW may be potential therapies targeting the prevention and cure of cardiac hypertrophy and fibrosis, which finally causes sudden heart failure.

No abstract

Renal ischemia-reperfusion (I/R) injury is an important cause of acute renal failure (ARF). Geumgwe-sinkihwan (GSH) was recorded in a traditional Chines medical book named “Bangyakhappyeon” in 1884. GSH has been used for treatment for patients with diabetes and glomerulonephritis caused by deficiency of kidney yang and insufficiency of kidney gi. Here we investigate the effects of GSH in mice model of ischemic acute kidney injury. The mice groups are as follows; sham group: C57BL6 male mice, I/R group: C57BL6 male mice with I/R surgery, GSH low group: I/R + 100 mg/kg/day GSH, and GSH high group: I/R + 300 mg/kg/day GSH. Ischemia was induced by clamping both renal arteries and reperfusion. Mice were orally given GSH (100 and 300 mg/kg/day) during 3 days after surgery. Treatment with GSH significantly ameliorated creatinine clearance, creatinine, and blood urea nitrogen levels. Treatment with GSH reduced neutrophil gelatinase associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1), specific renal injury markers. GSH also reduced the periodic acid–Schiff and picro sirius red staining intensity in kidney of I/R group. Western blot and real-time RT-qPCR analysis demonstrated that GSH decreased protein and mRNA expression levels of the inflammatory cytokines in I/R-induced ARF mice. Moreover, GSH inhibited protein and mRNA expression of inflammasome-related protein including NLRP3 (NOD-like receptor pyrin domain-containing protein 3, cryoprin), ASC (Apoptosis-associated speck-like protein containing a CARD), and caspase-1. These findings provided evidence that GSH ameliorates renal injury including metabolic dysfunction and inflammation via the inhibition of NLRP3-dependent inflammasome in I/R-induced ARF mice.