Green tea catechins inhibit Porphyromonas gulae LPS-induced inflammatory responses in human gingival epithelial cells

ObjectivesTo determine the anti-inflammatory effects of green tea catechins in immortalized human gingival epithelial cells (Ca9-22) stimulated with Porphyromonas gulae lipopolysaccharide (LPS).MethodsCa9-22 cells were incubated with P. gulae LPS (10 μg/ml) with or without green tea catechins, epigallocatechin-3-gallate (EGCg), epigallocatechin (EGC), epicatechin-3-gallate (ECG), and epicatechin (EC) (each at 50 μM), for 6 or 24 h. Real-time polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay were used to determine the induction of cyclooxygenase 2 (COX2), tumor necrosis factor alpha (TNF-ɑ), interleukin 6 (IL-6), and IL-8. Furthermore, the expression of toll-like receptors (TLRs) 2 and 4 was examined using real-time PCR and western blotting analysis, and phosphorylation of the p38 and ERK1/2 was examined using western blotting analysis.ResultsAt the mRNA and protein levels, EGCg, EGC, ECG, and EC were found to significantly inhibit COX2, TNF-ɑ, IL-6, and IL-8. Furthermore, the levels of ERK1/2 and p38 phosphorylation induced by P. gulae LPS were decreased following the addition of each of the catechins, as well as TLR2 and 4 mRNA and protein.ConclusionsThese findings indicate that green tea catechins are potent inhibitors of in?ammatory responses induced by P. gulae LPS, and may also be useful for prevention and/or attenuation of periodontitis.     

紫萁贯众单体成分对小鼠SIRS模型的保护作用

目的:建立小鼠全身炎症反应综合征(SIRS)模型,探索紫萁贯众醇提取物中单体成分对羟基苄叉丙酮(4-hydroxybenzylideneacetone,HBAc),3,4-二羟基苄叉丙酮(3,4-dihydroxybenzylideneacetone,DHBAc)对SIRS模型小鼠的保护作用及机制。方法:BALB/c小鼠随机分为正常组,模型组,HBAc,DHBAc低、中、高剂量(25,50,100μg·kg~(-1))组。预防给药7 d后腹腔注射脂多糖(LPS),造模5 h后检测小鼠肛温、呼吸频率、白细胞、血小板计数、白细胞分类、糖脂代谢以及肺组织炎症因子和炎症相关蛋白磷酸化情况。结果:与正常组比较,模型组小鼠腹腔注射LPS(6 mg·kg~(-1))可致小鼠呼吸频率降低(P0.05),体温明显降低(P0.01),外周血白细胞数和单核细胞百分比增加(P0.01),血小板减少(P0.01),血糖水平降低(P0.05),肺组织中白细胞介素-1β分泌增多(P0.01)。与模型组比较,HBAc,DHBAc均明显增加动物呼吸频率,升高动物体温,降低外周白细胞水平以及单核细胞百分比(P0.05,P0.01),并显著升高血糖水平(P0.05,P0.01),减少肺组织中白细胞介素-1β的分泌(P0.01)。结论:腹腔注射LPS致小鼠SIRS模型成立,HBAc,DHBAc对LPS致小鼠SIRS模型有一定的保护作用,可能通过IκB,c-JUN通路发挥抗炎作用。     

芒针对脊髓损伤大鼠运动功能和炎症水平的影响

目的探究芒针深刺秩边穴对大鼠脊髓损伤后运动功能的影响及可能作用机制。方法选择健康雄性Wister大鼠81只,随机分为正常组、模型组和芒针组(正常组9只,其余两组各36只),采用改良Allen's造模法制备大鼠脊髓中度损伤模型,模型组不做特殊处理,芒针组采用芒针深刺秩边穴,每日1次,每次30 min。分别于术后1 d、3 d、5 d、7 d行BBB(Basso-Beattie-Bresnahan)运动功能评分;术后1 d、3 d、5 d、7 d取受损段脊髓组织行酶联免疫吸附测定(ELISA)、实时荧光定量PCR(RT-qPCR)和苏木素-伊红染色(HE染色)。结果术后5 d和7 d,芒针组大鼠BBB评分高于模型组,差异有统计学意义(P<0.01);脊髓损伤后,模型组和芒针组大鼠脊髓组织中高迁移率族蛋白B1(HMGB1)、核转录因子kB(NF-kB)、白介素-6(IL-6)含量及HMGB1mRNA、NF-kBmRNA、IL-6mRNA水平显著升高(P<0.05);受损的脊髓组织松散,灰质中有许多空洞形成,伴有炎性细胞浸润。芒针治疗后,芒针组大鼠脊髓组织中HMGB1、NF-kB、IL-6含量及HMGB1mRNA、NF-kBmRNA、IL-6mRNA水平较模型组降低,且在3 d、5 d、7 d差异有统计学意义(P<0.05);受损部位的空洞及炎性细胞逐渐减少。结论脊髓损伤后,炎症因子的大量聚集引起级联性炎症反应,影响大鼠运动功能的恢复。芒针的抗炎机制可能包括抑制HMGB1的表达,降低NF-kB信号通路的传导,下调促炎因子IL-6的分泌。     

Prenatal exposure to perfluoroalkyl substances,immune-related outcomes,and lung function in children from a Spanish birth cohort study

BackgroundPrenatal exposure to perfluoroalkyl substances (PFASs) has been associated with impaired immune and respiratory health during childhood but the evidence is inconsistent and limited for lung function. We studied the association between prenatal PFASs exposure and immune and respiratory health, including lung function, up to age 7 years in the Spanish INMA birth cohort study.MethodsWe assessed four PFASs in maternal plasma samples collected during the 1st trimester of pregnancy (years: 2003–2008): perfluorohexane sulfonate (PFHxS), perfluorooctane sulfonate (PFOS), perfluorooctanoate (PFOA), and perfluorononanoate (PFNA). Mothers reported the occurrence (yes/no) of lower respiratory tract infections, wheezing, asthma, and eczema in the previous 12 months at 1.5 and 4 years of the child (n = 1188) and at 7 years (n = 1071). At ages 4 (n = 503) and 7 (n = 992) years lung function was assessed using spirometry tests.ResultsThe most abundant PFASs were PFOS and PFOA (geometric means: 5.80 and 2.31 ng/mL, respectively). The relative risk of asthma during childhood per each doubling in PFNA concentration was 0.74 (95 CI%: 0.57, 0.96). The relative risk of eczema during childhood per every doubling in PFOS concentration was 0.86 (95 CI%: 0.75, 0.98). Higher PFOA concentrations were associated with lower forced vital capacity and lower forced expiratory volume in 1 s z-scores at 4 years [β (95 CI %): −0.17 (−0.34, −0.01) and −0.13 (−0.29, 0.03), respectively], but not at 7 years.ConclusionThis longitudinal study suggests that different PFASs may affect the developing immune and respiratory systems differently. Prenatal exposure to PFNA and PFOS may be associated with reduced risk of respiratory and immune outcomes, particularly asthma and eczema whereas exposure to PFOA may be associated with reduced lung function in young children. These mixed results need to be replicated in follow-up studies at later ages.