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Objective. Inflammation is one of the key mechanisms involved in functional impairment after stroke. Intercellular adhesion molecule-1 (ICAM-1) is an important inflammatory molecule in the body. The purpose of our study was to determine the correlation between ICAM-1 and the prognosis of acute ischemic stroke (AIS). Methods. 286 AIS patients treated at Beijing Tiantan Hospital were continuously included in the study. The demographic data of the patients were collected, and the fasting blood within 24 hours of admission was collected to detect the clinical indicators. The functional prognosis was measured using the modified Rankin Scale (mRS) 3 months after stroke. The poor prognosis is defined as mRS ≥ 3. The enzyme-linked immunosorbent assay (ELISA) was used to determine the serum ICAM-1 levels. Results. The serum ICAM-1 levels of patients with poor prognosis were significantly higher than that of patients with good prognosis (144.2 ± 14.8 vs 117.5 ± 12.1 pg/ml). Receiver operating characteristic curve (ROC) analysis showed that the sensitivity and specificity of serum ICAM-1 for predicting the prognosis of AIS were 74% and 76%, respectively. In logistic regression analysis, the serum ICAM-1 level is still an independent predictor of poor prognosis (odds ratio [OR]: 0.52; 95% confidence interval [CI]: 0.318-0.839). Conclusions. Higher serum ICAM-1 levels on admission in AIS patients might increase the risk of poor prognosis. [ABSTRACT FROM AUTHOR]

In parallel with the prevalence metabolic syndrome, nonalcoholic fatty liver disease (NAFLD) has become the most common chronic liver disease in most countries. It features a constellation of simple steatosis, nonalcoholic steatohepatitis (NASH), fibrosis, cirrhosis, and even hepatocellular carcinoma. There are no approved drugs for effective management of NAFLD and NASH. Jianpi Huoxue formula (JPHX) mainly consists of Atractylodes macrocephal (Baizhu), Salvia miltiorrhiza (Danshen), Rasux Paeonia Alba (Baishao), Rhizoma Alismatis (Zexie), and Fructus Schisandrae Chinensis (Wuweizi), which may have beneficial effects on NAFLD. The aim of the study was to identify the effect of JPHX on NAFLD. A NAFLD model was induced by methionine-choline-deficient food (MCD) in Wistar rats and orally administered with simultaneous JPHX, once a day for 8 weeks. Hepatocellular injury, lipid profile, inflammation, fibrosis, and apoptosis were evaluated. The results showed that JPHX significantly decreased the abnormal serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels compared with the MCD model (P<0.05). Furthermore, JPHX protected MCD diet-fed rats from accumulation of hepatic triglycerides (TG) and total cholesterol (TC). Histological examination demonstrated that JPHX noticeably normalized the NAFLD activity score (NAS). Moreover, JPHX ameliorated liver inflammation by decreasing TNF-α levels and reduced collagen and matrix metalloproteinases in MCD diet-fed rats. In addition, JPHX prevented rats from MCD-induced cellular apoptosis, as suggested by TUNEL staining, and suppressed the activation of caspase 3 and 7 proteins. JPHX also inhibited the phosphorylation of JNK. In conclusion, JPHX exhibited a hepatoprotective effect against NAFLD in an MCD experimental model. [ABSTRACT FROM AUTHOR]

Rheumatoid arthritis (RA) is a widespread inflammatory disease whose clinical manifestations are joint swelling, pain, and disability, affecting approximately 1% of individuals worldwide. Conventional anti-RA drugs currently used in clinic have severe side effects. The present study is aimed at investigating the antiarthritic effects of total saponins from Nigella glandulifera seeds (TSNGS) in rats with adjuvant-induced rheumatoid arthritis (AIA). Arthritis score, paw swelling, and body weight were monitored throughout the period of TSNGS treatment. The histopathological features and levels of cytokines, including IFN-γ, TNF-α, IL-1β, IL-4, IL-6, IL-10, and IL-17A, and OPG/RANKL signaling, were measured to determine the amelioration by TSNGS and its potential mechanisms on the inflammatory response and bone erosion. The differentiation of regulatory T cells (Tregs) in serum was assessed by flow cytometry. The results demonstrate that TSNGS at 10 mg/kg, 50 mg/kg, and 250 mg/kg inhibited AIA-induced clinical score, paw swelling, and histological changes. TSNGS reduced the immune-inflammatory reaction by restoring the secretion and expression of inflammatory cytokines and elevating the proportion of CD4+ CD25+ Tregs, accompanied by an increase in transcription factor Foxp3 levels. TSNGS also displayed bone protection by upregulation of the OPG/RANKL pathway. Collectively, TSNGS inhibited arthritis in AIA rats and so represents a potential novel treatment for RA. [ABSTRACT FROM AUTHOR]