Antiplatelet drug ticagrelor delays gastric ulcer healing in rats.

Adenosine diphosphate P2Y12 receptor antagonist clopidogrel is not sufficiently safe for the gastric mucosa in patients with high risk of peptic ulcer, since it may impair healing of gastric erosions. However, the safety of the novel P2Y12 receptor antagonist ticagrelor in the gastric mucosa has not been elucidated to date. The present study aimed to examine whether ticagrelor delays gastric ulcer healing and to elucidate the involved mechanisms. Gastric kissing ulcers were produced in rats by luminal application of acetic acid solution, and ticagrelor was administered at dose of 10 or 20 mg/kg/day orally for 7 days. On day 8 after ulcer induction, the ulcer size, mucosal epithelial cell proliferation of the ulcer margin, expression levels of epidermal growth factor (EGF) and vascular endothelial growth factor (VEGF), and signal transduction pathways for cell proliferation and angiogenesis were measured and compared between the ticagrelor-treated and untreated model groups. The results revealed that the ulcer size was significantly greater in the ticagrelor-treated group compared with the model group, while the mucosal epithelial cell proliferation of the ulcer margin was significantly decreased in the ticagrelor-treated group. In addition, ticagrelor significantly decreased the ulcer-stimulated expression levels of EGF, VEGF, phosphorylated extracellular signal-regulated kinase (ERK), phosphorylated P38 mitogen-activated protein kinase and nuclear factor-κB P65 at the ulcer margin (P<0.05). These findings suggested that ticagrelor delayed gastric ulcer healing. Furthermore, the possible mechanisms underlying the effect of ticagrelor were associated with its functions of attenuating the expression levels of VEGF and EGF, as well as suppressing the phosphorylation activation of ERK1/2, P38 and nuclear factor-κB P65. Finally, the gastric epithelial cell proliferation and angiogenesis were also inhibited.

Protective potential of the methanol extract of Macrothelypteris oligophlebia rhizomes for chronic non-bacterial prostatitis in rats.

The protective potential of the methanol extract of Macrothelypteris oligophlebia rhizomes (MMO) for chronic non-bacterial prostatitis (CNP) in rats was investigated in the present study. Carrageenan-induced CNP in rats was established. Fifty rats were randomly divided into sham-operated (sham-ope) group, model group, positive control group (Cernilton at a dose of 148mg/kg body weight) and two MMO-treated groups (MMO at doses of 600mg/kg and 300 mg/kg body weight). The anti-prostatitis effect was evaluated by prostate index, the levels of interleukin-10 (IL-10), tumor necrosis factor alpha (TNF-α), cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE2), and histopathological examination. After 20 days of administration, MMO could significantly decrease prostate index and the levels of IL-10, TNF-α COX-2 and PGE2 in serum and could improve the prostate morphology in comparison with the model group. In summary, these results suggest that MMO possesses protective effects on prostate, which might be beneficial to further development for the treatment of CNP.

Hypolipidemic and anti-inflammatory properties of Abacopterin A from Abacopteris penangiana in high-fat diet-induced hyperlipidemia mice.

This study was to investigate the hypolipidemic and anti-inflammatory properties of Abacopterin A (APA), a flavonoid compound isolated from Abacopteris penangiana (Hook.) Ching. Male C57BL/6J mice were divided randomly and equally into five groups: the normal control group (N), the model group (M), the positive control group (P), the high and low doses of APA treated groups (H and L). All the animals except that in N group were fed with high-fat diet for 8 weeks. In the last 4 weeks, the mice in P, H and L groups were orally administered with simvastatin (at the dose of 20mg/kg/day) and APA (at the dose of 40 or 20mg/kg/day), respectively. Then the lipid profiles and related biochemical criterions of the studied mice were determined. The effects of high-fat diet on activating nuclear transcription factor-κB (NFκB) expression, elevating inflammatory factors tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) levels, and increasing triacylglycerol (TG) and total cholesterol (TC) levels were abolished on daily supplementation with APA. APA also enhanced lipoprotein lipase (LPL) and hepatic lipase (HL) activities. These results suggested that APA had hypolipidemic and anti-inflammatory properties through inhibiting NFκB expression, and reducing inflammatory response.

Parathelypteriside attenuates cognition deficits in d-galactose treated mice by increasing antioxidant capacity and improving long-term potentiation.

Parathelypteriside (PG), a stilbenoid compound, was extracted from Parathelypteris glanduligera (kze.) ching that exhibits antioxidative and anti-inflammatory effects. The aim of this study was to investigate the protective effect of PG against the d-galactose (d-gal)-induced neurotoxicity in mice. It was found that long-term intraperitoneal (i.p.) injection of PG (5 or 10 mg/(kg day)) for two weeks significantly improved the behavioral performance of d-gal-treated mice in both Morris water maze test and step-down avoidance test. Biochemical examination revealed that PG reduced the increased levels of malondialdehyde (MDA), and attenuated the decreased activities of superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase in the hippocampus of d-gal-treated mice. Furthermore, the electrophysiological assay showed that PG significantly rescued the long-term potentiation (LTP) impairment in mice hippocampus, and western blotting analysis indicated that the effects of PG on LTP might be attributed to the activation of cAMP-response element-binding protein (CREB). Together, these results suggested that the natural product PG represented a potential source of medicine for the treatment of the neurodegenerative diseases.