Pei-Lan Yu

Zhongnan University Of Technology, Ch’ang-sha-shih, Hunan, China

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Publications (5)1.22 Total impact

  • Ding-an Mao · Pei-lan Yu · Yu-jia Yang
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    ABSTRACT: To investigate the changes of interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) in the brain tissue of rats with infectious brain edema (IBE) and their relationship with heat shock protein 70 (HSP70) by heat stress response (HSR). Seventy-two SD rats were randomly divided into normal controls group (NS group), IBE group, and HSP group, each group was divided into three subgroups. The rats in subgroups were killed at 4 hours, 8 hours and 24 hours after the injections of IBE or normal saline respectively. HSP70 in brain tissues were determined by western blot analysis. The concentrations of IL-1beta and TNF-alpha in the brain homogenate of rats were determined by enzyme linked immunoadsorbent assay (ELISA). The results showed that HSP70 in brain tissues were elevated after heat shock. IBE group and NS group at 4 hours, 8 hours, 24 hours were induced to base levels of HSP70. The concentrations of TNF-alpha were significantly elevated in IBE group than in NS group at the various time points (P<0.01 or P<0.05), especially at 8 hours. The concentrations of IL-1beta were significantly increased in IBE group compared with NS group at 4 hours, 8 hours. HSR reduced the IL-1beta and TNF-alpha concentrations in the brain tissue in compared with IBE group (P<0.05 or P<0.01). IL-1beta and TNF-alpha are involved in infectious brain edema by IBE. HSP70 against infectious brain edema in rats may be associated with the reduction of IL-1beta and TNF-alpha in brain tissue.
    No preview · Article · Oct 2003 · Zhongguo wei zhong bing ji jiu yi xue = Chinese critical care medicine = Zhongguo weizhongbing jijiuyixue
  • Fei Yin · Yu-jia Yang · Pei-lan Yu
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    ABSTRACT: To study the possible mechanism of protective effect for Baicalin on Bacillus pertussis (BP) infected brain tissue and the dose-effect relationship. Brain tissues slices were divided into 7 groups: (1) the normal group; (2) the model group: infected by 10% BP; (3) the baicalin group, which was pretreated with baicalin, infected by BP and subdivided into 5 sub-groups according to different doses of baicalin used; (4) the glutamic acid group: cultured with glutamic acid; (5) the baicalin plus glutamic acid group; (6) the peroxide group: cultured with hydrogen peroxide; and (7) the baicalin plus peroxide group. The lactate dehydrogenase (LDH) content in the supernatant of culture was determined and quantitative protein determination was conducted. The LDH releasing was higher in the model group, glutamic acid group and peroxide group as compared with that in the normal group, 15.10 +/- 4.89 u/g. protein (the same unit below), 15.49 +/- 5.66 and 16.54 +/- 5.47 vs 6.10 +/- 2.87 respectively (P < 0.01). After being pretreated with 0.25 mmol/L baicalin, LDH level decreased significantly to 8.65 +/- 2.43, which was significantly different from that in the model group (P < 0.01), LDH was also decreased in the baicalin plus glutamic acid group (9.93 +/- 2.89) and baicalin plus peroxide group (9.54 +/- 2.82), which was significantly lower than that in the glutamic acid group and the peroxide group respectively (P < 0.01). Pretreatment of baicalin has protective effect on BP caused nerve cell injury in rat brain slices, the protection is possibly related with the reduction of glutamic acid and hydrogen peroxide induced damage on nerve cells in vitro.
    No preview · Article · Apr 2002 · Zhongguo Zhong xi yi jie he za zhi Zhongguo Zhongxiyi jiehe zazhi = Chinese journal of integrated traditional and Western medicine / Zhongguo Zhong xi yi jie he xue hui, Zhongguo Zhong yi yan jiu yuan zhu ban
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    ABSTRACT: Objective: To observe the effect of Qingkailing (QKL) on brain damage induced by glutamate, in order to seek for effective drugs for antagonizing neurotoxicity of glutamate.Methods:The number and morphological metrology of neurocytes in cerebral cortex and hippocampus were detected by MIAS-300 image analyser, electron microscope and immunohistochemical methods.Results: QKL could alleviate the glutamate induced accumulation of water and sodium in brain tissue, relieve the metrological and structural damage of cerebral cells in cortex and hippocampus, reduce the percentage of c-fos positive cell in brain.Conclusion: QKL could protect brain damage induced by glutamate, which might be related to the inhibition of QKL on the enhancement of cfos gene expression induced by glutamate.
    No preview · Article · Jan 2001 · Chinese Journal of Integrated Traditional and Western Medicine
  • Shao-Jie Yue · Pei-Lan Yu · Yu-Jia Yang · Zi-Qiang Luo
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    ABSTRACT: Objective: To observe the effect of 654-2 on brain edema model induced by pertussis bacilli in rabbits.Methods: Brain edema model of 26 rabbits induced by pertussis bacilli was prepared for observation, their brain water content and brain glutamate level were determined before and after treatment.Results: 654-2 could decline the water content of brain and increase the glutamate level in brain tissue of the treatment group as compared with group without treatment.Conclusion: 654-2 has protective effect on brain edema induced by pertussis bacilli.
    No preview · Article · Mar 1997 · Chinese Journal of Integrated Traditional and Western Medicine
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    ABSTRACT: This study aimed to evaluate the effect of tetramethylpyrazine in treating bacterial meningitis. Experimental model of rabbit meningitis was induced by intracisternal inoculation of 2 x 107 colony-forming units of Escherichia Coli and tumor necrosis factor-α, thromboxane B2 and 6-keto-prostagladin F1α concentrations in cerebrospinal fluid of rabbits in different treatment groups were measured at 24 hrs, 27 hrs and 30 hrs after infection. Results showed that tetramethylpyrazine could significantly lower the concentrations of tumor necrosis factor-α and thromboxane B2 in cerebrospinal fluid. Administration of both tetramethylpyrazine and ampicillin could attenuate the antibiotic-induced rapid release of the 2 inflammatory mediators.
    No preview · Article · Jan 1996 · Chinese Journal of Integrative Medicine