Intimal Hyperplasia of Arteriovenous Fistula.

Intimal hyperplasia (IH), a crucial histopathological injury, forms the basis of vascular stenosis and thrombogenesis. In addition, it is common in maladies such as stenosis at the anastomosis of arteriovenous fistula and restenosis after angioplasty. Various cellular and noncellular components play critical parts in the advancement of IH. This article reviews the distinctive components of IH, such as endothelial dysfunction, multiplication, and movement of vascular smooth muscle cells. Finally, in addition to synthesis of large amounts of extracellular matrix and inflammatory responses, which have frequently been studied in recent years, we offer a premise for clinical treatment with vascular smooth muscle cells.

Endoplasmic reticulum stress mediates parathyroid hormone-induced apoptosis in vascular smooth muscle cells.

Vascular calcification is one of the most common complications of chronic kidney disease (CKD), which is closely associated with increased mortality and morbidity rates of CKD patients. It has been reported that increased parathyroid hormone (PTH) aggravates vascular calcification in CKD patients. However, the direct role of PTH in vascular smooth muscle cells (VSMCs) is less elucidated. Here, we present evidence that PTH promotes apoptosis of VSMCs and endoplasmic reticulum (ER) stress participates in this process. Human aorta vascular smooth muscle cells (HASMCs) were treated with different concentrations of PTH for various time. HASMC apoptosis was detected by flow cytometry. Expression of phosphorylated (p)-PERK, CHOP, IRE1, p-JNK, and cleaved caspase 3 was determined by Western blotting. We found that PTH induced HASMC apoptosis and increased the expression of cleaved caspase 3. Furthermore, PTH activated PERK-CHOP and IRE1-JNK ER stress pathways. Either inhibition of JNK by SP600125 or CHOP by siRNA ameliorated PTH-induced apoptosis in HASMCs. We therefore suggest that ER stress participates in PTH-induced apoptosis of VSMCs, which may be a possible mechanism of PTH-promoted vascular calcification in CKD patients.

The effect of Bailing capsules combined with losartan to treat diabetic glomerulosclerosis and the combination's effect on blood and urine biochemistry.

OBJECTIVE: This study aimed to explore the efficacy of Bailing capsules combined with losartan to treat diabetic glomerulosclerosis (DG) and the combination's effect on blood and urine biochemistry. METHODS: 160 DG patients admitted to our hospital were recruited as the study cohort and randomly divided into a control group and an observation group (n=80 in each group). The control group was treated with losartan, and the observation group was treated with losartan and Bailing capsules. The efficacy, diastolic blood pressure (DBP), systolic blood pressure (SBP), blood creatinine (Scr), 24 h urine protein (24 h UP), blood urea nitrogen (BUN), urine microalbumin (mALB), urine ß2 microglobulin (ß2-MG), glomerular filtration rates (GFR), TCM scores, serum superoxide dismutase (SOD), reactive oxygen species (ROS), 8-hydroxydeoxyguanine (8-OHdG), hypersensitive C-reactive protein (hs-CRP), transforming growth factor ß1 (TGF-ß1), and the serum amyloid A (SAA) levels were compared between the two groups. RESULTS: The overall effective rate was higher in the observation group (91.25%) than it was in the control group (78.75%) (P<0.05). After the treatment, the DBP, SBP, Scr, 24 h UP, BUN, mALB, and ß2-MG levels were lower, and the GFR was higher in the observation group than in the control group (P<0.01). The TCM points were lower in the observation group than they were in the control group (P<0.01). The observation group also showed higher serum SOD and lower ROS, 8-OHdG, hs-CRP, TGF-ß1, and SAA levels than the control group (P<0.01). The differences in the incidences of adverse reactions between the two groups were not significantly different (P>0.05). CONCLUSION: Bailing capsules combined with losartan in the treatment of diabetic glomerulosclerosis can improve the therapeutic efficacy, improve the blood and urine biochemical indexes, the renal function, and the clinical symptoms, reduce the oxidative stress, improve the microinflammatory state, and delay the progression of the disease without increasing the adverse reactions.