At present, the treatment of hyperuricemia is designed primarily to decrease the production of uric acid using xanthine oxidase inhibitors; however, the therapeutic effect is not satisfactory. Therefore, the key to the successful treatment of hyperuricemia is to increase the excretion of uric acid. The aim of present study was to construct uricase-expressing genetically engineered bacteria and analyze the effects of these engineered bacteria on the lowering of uric acid levels in a rat model of hyperuricemia. The uricase expression vector was constructed by gene recombination technology and transfected into Escherichia coli. The expression and activity of uricase were analyzed by SdS-PAGE analysis and Bradford assay. The water consumption, food intake, body weight, eosinophil count and intestinal histology, in addition to the levels of serum uric acid (SUA) and allantoin in the feces of the rats, were assessed. The intestinal contents of the rats were analyzed by 16S rdNA sequencing technology. The results demonstrated that uricase-expressing genetically engineered bacteria secreted active uricase. All rats exhibited a natural growth trend during the entire experiment, and the SUA of hyperuricemic rats treated with uricase-expressing engineered bacteria was significantly decreased. In conclusion, these results indicate that uricase secreted by recombinant uricase-expressing genetically engineered bacteria served an important role in decreasing SUA levels in a rat model of hyperuricemia.

Primary brainstem hemorrhage (PBH) has the worst prognosis of all types of intracerebral hemorrhage. Currently, the management of PBH is controversial. Hematoma classification, scoring systems, and electrophysiological monitoring are critical for predicting the outcome of PBH. Surgery may be an effective treatment for PBH. Clinical studies have emphasized the importance of animal models for understanding the pathogenesis and pathological mechanisms of PBH. In this study, combined with recent studies, the outcome prediction, surgical treatment, and animal models of PBH were reviewed.

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