ABSTRACT
In this research, the degradation behavior and failure mechanism of silicone rubber seal rings under the synergistic effects of multiple factors in the marine atmosphere are fully investigated. Firstly, four aging factors of air, temperature, compressive stress, and chemical medium were determined by analyzing the service environment profile of silicone rubber seal under a marine atmosphere environment. Secondly, to better simulate the actual service environment of silicone rubber and shorten the test period, an artificially accelerated aging test was designed and carried out in the laboratory. In this paper, temperature is utilized as the accelerating stress. According to the results of the pre-test, the accelerating stress level is finally determined to be 110-150 ∘C. In addition, the compression set applied is consistent with the constant compression permanent deformation value of 28% of the silicone rubber in the actual service process. Finally, through the macroscopic physical properties and microstructure analysis of the samples before and after aging, the corresponding test results are given, and the failure mechanism is analyzed and discussed in detail. Through the above test results and discussion, it can be concluded that the aging process of multi-factor coupling on the lower silicone rubber seal ring is uneven, and its aging process is not a simple superposition of multiple environmental factors. More importantly, the above test data and results are of great significance for evaluating the service life of silicone rubber seals, which can be utilized in the future to improve the reliability and durability of related equipment in the marine environment.
ABSTRACT
AIM: Sitagliptin (Sita) is a dipeptidyl peptidase-4 inhibitor which has been approved as a curing medicine for Type 2 diabetes (T2D) and has also reported its neuroprotective and antioxidant activity. This article describes the therapeutic eï¬ects of Sita on induced rat model of SE by kainic acid (KA) and investigated the antioxidative pathway of sita. METHODS: Sprague-Dawley male rats were used randomly divided in four groups: vehicle control, KA and Sita + KA in a 5 and 10 mg/kg doses respectively in further groups. SE in rats was induced by the administration of KA in Phosphate buffered saline (PBS) intraperitoneally (IP) in a dose of 15 mg/kg. Seizure intensity, oxidative stress parameters, TUNEL assay, histopathology, and Nrf2/HO-1 expressions were evaluated. RESULTS: Increment in the latency in SE results in delaying the initiation of disease in the pretreated rats by Sita compared to induce group (KA) as well the percentage of occurrence of SE was decreased. The content of MDA elevates whereas the SOD production decreases on administering the KA at various time intervals. Sita shows protective action against the KA-induced SE by reducing the oxidative stress thus inhibiting the change in SOD and MDA was observed after KA administration prior SE onset. Based on the above results, the study explains possible molecular mechanism of Sita. Sita Pretreatment showed significant elevation in expression of Nrf2 and HO-1 proteins in hippocampus region of the brain. CONCLUSION: Above parameters defines the potential effect of Sita on brain injury occurred due to SE by anti-oxidative pathway.
