This study aimed to investigate the therapeutic effect of berberine on renal ischemia-reperfusion injury in rats and its effect on Bax and Bcl-2. Sixty adult SD rats were randomly divided into four groups: control group A, renal ischemia-reperfusion group B, berberine group C and berberine + exendin-(9–39) treatment group D. In group A, right kidney was resected and left renal pedicle was separated, but left renal artery was not blocked. Renal ischemia-reperfusion model was established in other groups. Rats in group C were not subjected to any treatment after model construction. Rats in group C and D were subjected to intraperitoneal injection of berberine 7 days before the experiment. Besides that, intraperitoneal injection of exendin-(9–39) was performed at day 1 and 4 after model construction. Automatic biochemical analyzer was used to measure serum creatinine (SCr) and blood urea nitrogen (BUN). Malondialdehyde (MDA) in renal cortex was measured by enzyme-linked immunosorbent assay and contents of Bax and Bcl-2 in renal tissue were measured by western blot analysis. Apoptosis of rat renal cells was detected by TUNEL assay. The results showed that levels of SCr, BUN, MDA and Bax were significantly higher in group B than in other groups (P<0.05). Levels of Bcl-2 in group B were significantly higher than those in group A but significantly lower than those in group C and D. Compared with group A, apoptosis of renal cells was more severe in group B. Compared with group B, apoptosis of renal cells was significantly improved in group C and D, but was still more severe than that in group A. In conclusion, berberine can effectively improve renal function in rats with renal ischemia-reperfusion injury by inhibiting Bax expression and promoting Bcl-2 expression.

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Existing evidences have emphasized an important role of oxidative stress in dexamethasone (Dex)-induced osteoblastic cell damages. Here, we investigated the possible anti-Dex activity of edaravone in osteoblastic cells, and studied the underlying mechanisms. We showed that edaravone dose-dependently attenuated Dex-induced death and apoptosis of established human or murine osteoblastic cells. Further, Dex-mediated damages to primary murine osteoblasts were also alleviated by edaravone. In osteoblastic cells/osteoblasts, Dex induced significant oxidative stresses, tested by increased levels of reactive oxygen species and lipid peroxidation, which were remarkably inhibited by edaravone. Meanwhile, edaravone repressed Dex-induced mitochondrial permeability transition pore (mPTP) opening, or mitochondrial membrane potential reduction, in osteoblastic cells/osteoblasts. Significantly, edaravone-induced osteoblast-protective activity against Dex was alleviated with mPTP inhibition through cyclosporin A or cyclophilin-D siRNA. Together, we demonstrate that edaravone protects osteoblasts from Dex-induced damages probably through inhibiting oxidative stresses and following mPTP opening.

Background In this study, we aim to investigate the efficiency of artesunate (AS) on Echinococcus granulosus protoscoleces and metacestodes. Methods For the in vitro assay, the eosin dye exclusion test and transmission electron microscope (TEM) were utilized to evaluate the effects of AS against protoscoleces (PSCs) from Echinococcus granulosus . In addition, mortality, ultrastructure change, reactive oxygen species (ROS) content and DNA damage were measured in order to explore the anti-echinococcosis mechanism of AS. For the in vivo assay, CE-infected mice were divided into model group, albendazole (ABZ) group (200 mg/kg), low AS (AS-L) group (50 mg/kg), moderate AS (AS-M) group (100 mg/kg), and high AS (AS-H) group (200 mg/kg). Upon 6 weeks oral administration, wet weight of cysts and the ultrastructural changes of cystic wall were utilized to evaluate the effects of AS on metacestodes. In addition, the liver biochemical parameters, tumor necrosis factor-α (TNF-α), glutathione/glutathione oxidized (GSH/GSSG) ratio in serum, and H 2 O 2 , total superoxide dismutase (T-SOD) in cyst fluid were detected. Results Both in vivo and in vitro experiments showed that AS showed anti-parasitic effects on CE. The AS could elevate the ROS level in the PSCs, which then resulted in obvious DNA damages. AS could significantly improve the liver biochemical parameters in infected mice compared with the model group ( P < 0.05). Compared with the model group, AS-M and AS-H decrease the TNF-α content ( P < 0.05); AS-H group significantly decrease in the serum GSH/GSSG ratio ( P < 0.05). The content of H 2 O 2 in hydatid fluid treated by AS showed significant decrease compared with the model group ( P < 0.01), while the T-SOD level showed significant elevation compared with model group ( P < 0.01). Conclusion In this study, we confirmed that the effects of AS on Echinococcus granulosus protoscoleces and metacestodes may be related to the DNA damages induced by oxidative stress, which provided solid information for the research and development of drugs for cystic echinococcosis.

Glutathione S-transferase gene polymorphism had no association with chemosensitivity in patients with osteosarcoma.