Safety of the Xuesaitong injection in China: results from a large-scale multicentre post-marketing surveillance study in a real-world setting.

OBJECTIVE: The safety profile of traditional Chinese medicine injections has emerged as the greatest challenge to their clinical application. The authors aimed to perform a post-marketing surveillance study in a real-world setting to evaluate the safety of the Xuesaitong (XST) injection in China. METHODS: This multi-centre, post-marketing, observational study enrolled patients who received XST injections in 42 centres in China between March 2015 and November 2017. Adverse drug reactions (ADRs) and adverse drug events (ADEs) were collected and evaluated in a post-marketing database. Logistic regression analysis was performed to analyse the risk factors for ADRs. RESULTS: A total of 30,008 consecutive patients with a mean age of 62.29 ± 14.58 years were included in this post-marketing study. The incidences of ADEs and ADRs were 0.5% and 0.33%, respectively. The most common clinical manifestations were damage to skin and appendages (47.66%). There were four new kinds of ADEs found in the present monitoring study. The majority of ADRs were type B (62.62%) and occurred within 24 h after XST injection treatment. No severe ADRs were reported in this analysis. Multivariate logistic regression analysis showed that the hospital level (OR = 0.607; 95% CI = 0.407-0.906; p = .0144), hypertension (OR = 1.979; 95% CI, 1.323-2.959; p = .0009) and solvent type (OR = 2.951; 95% CI, 1.608-5.417; p = .0005) were risk factors for ADR occurrence. CONCLUSION: XST injection is well tolerated and has a favourable safety profile for patients in a real-world setting. This post-marketing study provided further evidence of the safety of XST injections for clinical applications.

Cytotoxicity and apoptosis induction in human HepG2 hepatoma cells by decabromodiphenyl ethane.

OBJECTIVE: To investigate the toxic effects of decabromodiphenyl ethane (DBDPE), used as an alternative to decabromodiphenyl ether in vitro. METHODS: HepG2 cells were cultured in the presence of DBDPE at various concentrations (3.125-100.0 mg/L) for 24, 48, and 72 h respectively and the toxic effect of DBDPE was studied. RESULTS: As evaluated by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide and lactate dehydrogenase assays and nuclear morphological changes, DBDPE inhibited HepG2 viability in a time- and dose-dependent manner within a range of 12.5 mg/L to 100 mg/L and for 48 h and 72 h. Induction of apoptosis was detected at 12.5-100 mg/L at 48 h and 72 h by propidium iodide staining, accompanied with overproduction of reactive oxygen species (ROS). Furthermore, N-acetyl-L-cysteine, a widely used ROS scavenger, significantly reduced DBDPE-induced ROS levels and increased HepG2 cells viability. CONCLUSION: DBDPE has cytotoxic and anti-proliferation effect and can induce apoptosis in which ROS plays an important role.

Single-wall carbon nanotubes induce oxidative stress in rat aortic endothelial cells.

Oxidative stress is a major factor contributing to endothelial cell damage. Single-wall carbon nanotubes (SWCNTs) have oxidative properties; however, the oxidative effects of SWCNTs on endothelial cells are not fully understood. In the present study, we investigated the effects of oxidative stress induced by SWCNTs on rat aortic endothelial cells (RAECs). Various markers of cellular damage were assessed, such as biochemical and ES immunity indexes, and DNA and protein damage. Our findings suggest that RAEC endured oxidative damage following SWCNT exposure. Specifically, after SWCNTs exposure, non-enzymatic antioxidant glutathione was activated prior to superoxide dismutase activation in order to defend against oxidative stress. Additionally, it was found that as SWCNT concentration increased, so did the stress protein, heme oxygenase-1 (HO-1), expression levels. These changes may induce RAEC damage, and result in many serious diseases.

Abdominal fat accumulation with hyperuricemia and hypercholesterolemia quail model induced by high fat diet.

OBJECTIVE: To establish abdominal fat accumulation with hyperuricemia and hypercholesterolemia quail model fed with high fat diet. And then to investigate the pathological characteristics of this quail model. METHODS: Thirty Longcheng quails were randomly divided into two groups: control group and model group (n=15). The control group quails were fed with normal diet and model group quails were fed with high fat diet for 14 days. After a 12-hour overnight fast, liver and abdominal fat at euthanasia as well as serum were collected. The levels of serum uric acid, total cholesterol, high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), triglyceride, free fatty acid (FFA), and blood glucose were assayed. The activity changes of adenosine deaminase (ADA), xanthine oxidase (XOD), lipoprotein lipase (LPL), hepatic lipase (HL), and fatty acid synthetase (FAS) were analyzed. RESULTS: Compared with control group, the abdominal fat content (0.74+/-0.63 vs. 1.36+/-0.65 g, P<0.05) and abdominal fat index (0.44%+/-0.30% vs. 0.85%+/-0.30%, P<0.01) as well as live lipid index (3.61%+/-0.65% vs. 11.33%+/-2.14%, P<0.01) in model group significantly increased; the levels of serum uric acid (210.61+/-94.76 vs. 304.25+/-141.94 micromol/L, P<0.05), total cholesterol (4.20+/-0.51 vs. 20.10+/-11.25 mmol/L, P<0.01), LDL-C (1.16+/-0.29 vs. 10.78+/-6.48 mmol/L, P<0.01), and FFA (0.39+/-0.14 vs. 0.55+/-0.15 mmol/L, P<0.01) in model group significantly increased; HDL-C (5.85+/-0.95 vs. 4.14+/-2.03 mmol/L, P<0.05) significantly decreased; the levels of triglyceride and blood glucose had no significant changes (P>0.05); the activities of ADA (9.71+/-3.05 vs. 17.19+/-5.10 U/ml, P<0.01) and XOD (10.58+/-6.88 vs. 19.22+/-9.44 U/L, P<0.01) in model group significantly increased; and FAS, LPL, HL had no significant changes (P>0.05). CONCLUSIONS: High fat diet can induce abdominal fat accumulation with hyperuricemia and hypercholesterolemia quail model. The changes of uric acid and lipid metabolic enzyme activities may be the pathological mechanism of abdominal fat accumulation with hyperuricemia and hypercholesterolemia.