Maslinic acid prevents IL-1ß-induced inflammatory response in osteoarthritis via PI3K/AKT/NF-κB pathways.

Osteoarthritis (OA) is a degenerative joint disease characterized by destruction of articular cartilage. The inflammatory response is the most important factor affecting the disease process. As interleukin-1ß (IL-1ß) stimulates several key mediators in the inflammatory response, it plays a major role in the pathogenesis of OA. Maslinic acid (MA) is a natural compound distributed in olive fruit. Previous studies have found that maslinic acid has an inhibitory effect on inflammation, but its specific role in the progression of OA disease has not been studied so far. In this study, we aim to assess the protective effect of MA on OA progression by in vitro and in vivo experiments. Our results indicate that, in IL-1ß-induced inflammatory response, MA is effective in attenuating some major inflammatory mediators such as nitric oxide (NO) and prostaglandin E2, and inhibits the expression of IL-6, inducible nitric oxide synthase, cyclooxygenase-2, and tumor necrosis factor-α (TNF-α) in a concentration-dependent manner. Also, MA downregulated the expression levels of thrombospondin motif 5 (ADAMTS5) and matrix metalloproteinase 13 in chondrocytes, resulting in reduced degradation of its extracellular matrix. Mechanistically, MA exhibits an anti-inflammatory effect by inactivating the PI3K/AKT/NF-κB pathway. In vivo, the protective effect of MA on OA development can be detected in a surgically induced mouse OA model. In summary, these findings suggest that MA can be used as a safe and effective potential OA therapeutic strategy.

Silencing of Ref-1 expression by retrovirus-mediated shRNA sensitizes HEK293 cells to hydrogen peroxide-induced apoptosis.

Redox factor-1 (Ref-1) is a multifunctional protein involved in DNA base excision repair (BER) and transcription factor modification. By the use of retrovirus-delivered shRNA, we effectively suppressed endogenous Ref-1 expression in human embryonic kidney (HEK) 293 cells. Our results showed that downregulation of Ref-1 rendered cells more sensitive to H(2)O(2)-induced apoptosis. In this process, the absence of Ref-1 decreased the ratio of Bcl-2/Bax protein expression, which resulted in cytochrome c release and caspase-3 activation. These data indicate that constitutive Ref-1 is required for cellular defense and that this protective function is dependent on its role in the regulation of Bcl-2 family proteins.

[Corrosion of stainless steel 201, 304 and 316L in the simulated sewage pipes reactor].

The corrosion behavior of stainless steel 201, 304 and 316L which would be used as sewer in-situ rehabilitation materials was studied in the simulated sewage pipes reactor. The corrosion potential and corrosion rate of these three materials were studied by potentiodynamic method on the 7th, 14th, 21st, 56th day under two different conditions which were full immersion condition or batch immersion condition with a 2-day cycle. The electrode process was studied by Electrochemical Impedance Spectroscopy (EIS) on the 56th day. The microstructure and composition of the corrosion pitting were analyzed by Scanning Electron Microscope (SEM) and Energy Dispersive Spectrometer (EDS) on the 56th day. The results showed that 304 and 316L had much better corrosion resistance than 201 under both conditions. 304 and 316L had much smaller corrosion rate than 201 under both conditions. The corrosion resistance of all three kinds of stainless steel under the batch immersion condition was much better than those under the full immersion condition. The corrosion rate of all three kinds of stainless steel under the batch immersion condition was much smaller than those under the full immersion condition. Point pitting corrosion was formed on the surfaces of 304 and 316L. In comparison, a large area of corrosion was formed in the surface of 201.