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Underwater gliders are unmanned undersea vehicles that utilize hydrodynamic principles to glide through water. They rely on a range of technologies, including overall design principles such as hydrodynamic shape and pressure-resistant hull, specific unit technologies such as buoyancy-driven propulsion, attitude adjustment, energy management, intelligent control, and sensor integration, as well as application technologies such as path planning and collaborative networking. The deep-sea intelligent equipment team at Tianjin University has made significant advancements in the development of underwater gliders in China, having spent over 20 years since 2002 designing and refining their flagship model, the Petrel. This vehicle has achieved a high level of performance in critical areas such as working depth, endurance, and sensor integration. This review presents an overview of the key technologies, advanced methods, and innovative theories that have been used in the development of the Petrel series, including its overall design, buoyancy-driven propulsion system, energy management, collaborative networking, and sea trial applications. Additionally, we explore the potential of bionic technology to inform the future development of underwater glider technology. This review seeks to afford valuable insights that will inform the continued rapid advancement of unmanned undersea vehicle technology in China.

Objective LPS-treated PC12 cells were used to establish neuron inflammation model. RT-PCR was used to detect the mRNA of cytokines. CCK-8 assay was used to check determine cell viability. Western blot was used to detect NF-κB pathway. Methods LPS-treated PC12 cells were used to establish neuron inflammation model. RT-PCR was used to detect the mRNA of cytokines. CCK-8 assay was used to check determine cell viability. Western blot was used to detect NF-κB pathway. Results After 12 hrs treatment of PC12 cells with different doses of LPS (0, 100, 300 and 1 000 ng/mL), the mRNA level of TNF-α,IL-6 and IL-1β all increased. The cells pre-treated with different doses of gypenoside (30, 100 μg/mL) and then treated with LPS for 24 h, cell viability decreased to 85.7%. However, 30 and 100 μg/mL gypenoside pre-treatment resulted in cell viability increased to 96.2% and 97.9% respectively. Gypenoside also inhibited LPS-induced cell inflammation as indicated by increased mRNA level of TNF-α, IL-6 and IL-1β caused by LPS stimulation. LPS increased the phosphorylation of p65 (p-p65) and the phosporylation was also inhibited by gypenoside treatment. Conclusions Gypenoside alleviates LPS-induced inflammation and then protects PC12 cells from injury induced by LPS through inhibiting NF-κB pathway.