Puerarin protects against damage to spatial learning and memory ability in mice with chronic alcohol poisoning

We evaluated the effect of puerarin on spatial learning and memory ability of mice with chronic alcohol poisoning. A total of 30 male C57BL/6 mice were randomly divided into model, puerarin, and control groups (n=10 each). The model group received 60% (v/v) ethanol by intragastric administration followed by intraperitoneal injection of normal saline 30 min later. The puerarin group received intragastric 60% ethanol followed by intraperitoneal puerarin 30 min later, and the control group received intragastric saline followed by intraperitoneal saline. Six weeks after treatment, the Morris water maze and Tru Scan behavioral tests and immunofluorescence staining of cerebral cortex and hippocampal neurons (by Neu-N) and microglia (by Ib1) were conducted. Glutamic acid (Glu) and gamma amino butyric acid (GABA) in the cortex and hippocampus were assayed by high-performance liquid chromatography (HPLC), and tumor necrosis factor (TNF)-α and interleukin (IL)-1β were determined by ELISA. Compared with mice in the control group, escape latency and distance were prolonged, and spontaneous movement distance was shortened (P<0.05) by puerarin. The number of microglia was increased in both the cortex and hippocampal dentate gyrus (P<0.01), and neurons were reduced only in the hippocampal dentate gyrus (P<0.01) in puerarin-treated mice. In the model group, Glu and GABA levels decreased (P<0.05), and Glu/GABA, TNF-α, and IL-1β increased (P<0.01) with puerarin treatment, returning to near normal levels. In conclusion, puerarin protected against the effects of chronic alcohol poisoning on spatial learning and memory ability primarily because of anti-inflammatory activity and regulation of the balance of Glu and GABA.

Puerarin protects against damage to spatial learning and memory ability in mice with chronic alcohol poisoning.

We evaluated the effect of puerarin on spatial learning and memory ability of mice with chronic alcohol poisoning. A total of 30 male C57BL/6 mice were randomly divided into model, puerarin, and control groups (n=10 each). The model group received 60% (v/v) ethanol by intragastric administration followed by intraperitoneal injection of normal saline 30 min later. The puerarin group received intragastric 60% ethanol followed by intraperitoneal puerarin 30 min later, and the control group received intragastric saline followed by intraperitoneal saline. Six weeks after treatment, the Morris water maze and Tru Scan behavioral tests and immunofluorescence staining of cerebral cortex and hippocampal neurons (by Neu-N) and microglia (by Ib1) were conducted. Glutamic acid (Glu) and gamma amino butyric acid (GABA) in the cortex and hippocampus were assayed by high-performance liquid chromatography (HPLC), and tumor necrosis factor (TNF)-α and interleukin (IL)-1ß were determined by ELISA. Compared with mice in the control group, escape latency and distance were prolonged, and spontaneous movement distance was shortened (P<0.05) by puerarin. The number of microglia was increased in both the cortex and hippocampal dentate gyrus (P<0.01), and neurons were reduced only in the hippocampal dentate gyrus (P<0.01) in puerarin-treated mice. In the model group, Glu and GABA levels decreased (P<0.05), and Glu/GABA, TNF-α, and IL-1ß increased (P<0.01) with puerarin treatment, returning to near normal levels. In conclusion, puerarin protected against the effects of chronic alcohol poisoning on spatial learning and memory ability primarily because of anti-inflammatory activity and regulation of the balance of Glu and GABA.

Association between IL-1RN gene polymorphisms and susceptibility to ankylosing spondylitis: a large Human Genome Epidemiology review and meta-analysis.

We made a Human Genome Epidemiology review and meta-analysis to examine a possible association between interleukin-1 receptor antagonist (IL-1RN) polymorphisms and susceptibility to ankylosing spondylitis (AS). Studies of IL-1RN polymorphisms and susceptibility to AS were found by searching the Pubmed, Cochrane library, Embase, Web of Science, Springerlink, CNKI, and CBM databases. Data were extracted by 2 independent reviewers. The meta-analysis was performed with the Review Manager Version 5.1.6 and STATA Version 12.0 software. The odds ratio (OR) and 95% confidence intervals (95%CI) were calculated based on the extracted data. Thirteen studies with 5391 AS cases and 5239 healthy controls were retrieved. Seven IL-1RN polymorphisms were addressed, including rs30735, rs31017, rs419598, rs315951, rs315952, rs27810, and VNTR. Meta-analysis showed that the rs30735*C allele/carrier, the rs31017*G carrier and the rs315952*T carrier were positively and significantly associated with susceptibility to AS (OR = 1.45, 95%CI = 1.19-1.76; OR = 1.73, 95%CI = 1.34-2.24; OR = 1.30, 95%CI = 1.01-1.69; OR = 1.54, 95%CI = 1.16-2.04). A subgroup analysis based on ethnicity revealed significant positive associations between the rs30735*C allele/carrier and the rs31017*G allele and susceptibility to AS in both Caucasian and Asian populations, while the positive association between the rs315952*T carrier and AS susceptibility was significant only in Asian populations (OR = 1.54, 95%CI = 1.16-2.04). This meta-analysis suggests that IL-1RN polymorphisms are involved in the pathogenesis of AS. The rs30735*C allele/carrier, and the rs31017*G allele may be risk factors for ankylosing spondylitis in Caucasians and Asians, while the rs315952*T carrier is associated with susceptibility to this disease only in Asians.