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Aim： To investigate whether strontium ranelate （SR）, a new antiosteoporotic agent, could attenuate cartilage degeneration and sub- chondral bone remodeling in osteoarthritis （OA）. Methods： Medial meniscal tear （MMT） operation was performed in adult SD rats to induce OA. SR （625 or 1800 mg·kg^-1·d^-1） was administered via gavage for 3 or 6 weeks. After the animals were sacrificed, articular cartilage degeneration was evaluated using toluidine blue 0 staining, SOX9 immunohistochemistry and TUNEL assay. The changes in microarchitecture indices and tissue mineral density （TMD）, chemical composition （mineral-to-collagen ratio）, and intrinsic mechanical properties of the subchondral bones were measured using micro-CT scanning, confocal Raman microspectroscopy and nanoindentation testing, respectively. Results： The high-dose SR significantly attenuated cartilage matrix and chondrocyte loss at 6 weeks, and decreased chondrocyte apop- tosis, improved the expression of SOX9, a critical transcription factor responsible for the expression of anabolic genes type II collagen and aggrecan, at both 3 and 6 weeks. Meanwhile, the high-dose SR also significantly attenuated the subchondral bone remodeling at both 3 and 6 weeks, as shown by the improved microarchitecture indices, TMD, mineral-to-collagen ratio and intrinsic mechanical prop- erties. In contrast, the low-dose SR did not significantly change all the detection indices of cartilage and bone at both 3 and 6 weeks. Conclusion： The high-dose SR treatment can reduce articular cartilage degeneration and subchondral bone remodeling in the rat MMT model of OA.

Background： Tumor necrosis factor-α （TNF-α） plays an important role in progressive contractile dysfunction in several cardiac diseases. The cytotoxic effects of TNF-α are suggested to be partly mediated by reactive oxygen species （ROS）- and mitochondria-dependent apoptosis. Glucagon-like peptide- 1 （GLP-1） or its analogue exhibits protective effects on the cardiovascular system. The objective of the study was to assess the effects ofexenatide, a GLP- 1 analogue, on oxidative stress, and apoptosis in TNF-α-treated cardiomyocytes in vitro. Methods： Isolated neonatal rat cardiomyocytes were divided into three groups： Control group, with cells cultured in normal conditions without intervention; TNF-α group, with cells incubated with TNF-α （40 ng/ml） for 6, 12, or 24 h without pretreatment with exenatide; and exenatide group, with cells pretreated with exenatide （100 nmol/L） 30 mins before TNF-α （40 ng/ml） stimulation. We evaluated apoptosis by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling （TUNEL） assay and flow cytometry, measured ROS production and mitochondrial membrane potential （MMP） by specific the fluorescent probes, and assessed the levels of proteins by Western blotting for all the groups. Results： Exenatide pretreatment significantly reduced cardiomyocyte apoptosis as measured by flow cytometry and TUNEL assay at 12 h and 24 h. Also, exenatide inhibited excessive ROS production and maintained MMP. Furthermore, declined cytochrome-c release and cleaved caspase-3 expression and increased bcl-2 expression with concomitantly decreased Bax activation were observed in exenatide-pretreated cultures. Conclusion： These results suggested that exenatide exerts a protective effect on cardiomyocytes, preventing TNF-α-induced apoptosis; the anti-apoptotic effects may be associated with protection ofmitochondrial function.

Bifenthrin（BF） is a pyrethroid insecticide that is widely used in agriculture, horticulture, and for residential purposes. However, few studies addressing the reproductive toxicity of BF on fishes are available. The present study was conducted to investigate the effects of BF on testicular development in Sebastiscus marmoratus and to gain insight into its mechanism. After exposure to 1, 10 and 100 ng/L BF for 50 days, there was a reduced number of mature sperm and an abundance of the late stages of spermatocysts in the testes. The levels of 17β-estradiol and testosterone were decreased significantly after BF exposure. The activity of caspase-3 was increased in a dosedependent manner after BF exposure, TUNEL assay indicated that BF exposure resulted in the occurrence of apoptosis in the testes, which might be main reason for the inhibition of spermatogenesis.