背景:牙周炎是以牙菌斑生物膜为主要致病物质的炎症性、破坏性疾病,发生于牙龈、牙周膜、牙槽骨和牙骨质。细菌复合体的抗原及其分泌的毒素、酶等直接导致牙周组织的破坏,并引发宿主的免疫反应,使机体组织受到间接损害。沉默信息调节因...背景:牙周炎是以牙菌斑生物膜为主要致病物质的炎症性、破坏性疾病,发生于牙龈、牙周膜、牙槽骨和牙骨质。细菌复合体的抗原及其分泌的毒素、酶等直接导致牙周组织的破坏,并引发宿主的免疫反应,使机体组织受到间接损害。沉默信息调节因子(Sirtuins,SIRTs)在抗衰老、抗氧化应激、调节炎症、介导细胞自噬等方面发挥重要作用,与牙周炎的发生和发展也有着密切的关系。目的:针对Sirtuins在牙周炎中的研究概况做一综述。方法:由第一作者应用计算机在PubMed、Web of Science、中国知网和万方数据库检索涉及Sirtuins在牙周炎中的相关研究,以“Sirtuins,Sirtuin1-7,periodontitis”为英文检索词,“沉默信息调节因子,沉默信息调节因子1-7,牙周炎”为中文检索词,经过筛选后纳入57篇文献进行综述分析。结果与结论:①SIRT1、SIRT2、SIRT3、SIRT6参与调控了牙周炎的发生与发展;②SIRT1:抑制SIRT1表达可能是牙周炎治疗靶点;SIRT1的过表达对牙周炎症有抑制作用,保护牙周组织;SIRT1的激活剂可减轻牙周组织的炎症,并可改善牙周炎引起的全身组织病变;③SIRT2:参与烟酰胺磷酸核糖转移酶介导的牙周炎症,SIRT2在牙周疾病的治疗和转归中发挥一定的作用;④SIRT3:可改善年龄相关的牙周病;天麻素可通过SIRT3的上调促进牙周膜干细胞成骨分化;SIRT3的激活剂通过调节细胞自噬水平,降低牙周炎对牙周和肾脏组织的破坏程度;⑤SIRT6:可抑制牙周组织炎症反应,抑制成牙骨质细胞的分化和矿化;SIRT6对根尖周炎的预后有利;⑥SIRT4、SIRT5、SIRT7与牙周炎的关系鲜有报道。展开更多
背景:不同于非炎症性细胞凋亡,细胞焦亡是炎症性细胞死亡的一种形式,它伴随着膜完整性的破坏和促炎性细胞内物质的释放,因而与多种疾病有关。沉默信息调节因子家族是依赖于烟酰胺腺嘌呤二核苷酸的组蛋白去乙酰化酶家族。除了去乙酰化外...背景:不同于非炎症性细胞凋亡,细胞焦亡是炎症性细胞死亡的一种形式,它伴随着膜完整性的破坏和促炎性细胞内物质的释放,因而与多种疾病有关。沉默信息调节因子家族是依赖于烟酰胺腺嘌呤二核苷酸的组蛋白去乙酰化酶家族。除了去乙酰化外,还具有其他酶活性,如脱琥珀酸化、脱丙酰化和腺苷二磷酸-核糖基化等,在参与细胞焦亡调控中发挥重要的作用。目的:综述沉默信息调节因子家族在细胞焦亡中的作用及影响。方法:第一作者通过检索PubMed、Web of Science、中国知网、万方数据库,检索时限为各数据库建库至2024年3月,中文检索词为“沉默信息调节因子,沉默信息调节因子1,沉默信息调节因子2,沉默信息调节因子3,沉默信息调节因子4,沉默信息调节因子5,沉默信息调节因子6,沉默信息调节因子7,细胞焦亡”,英文检索词为“Sirtuins,Sirtuin1,Sirtuin2,Sirtuin3,Sirtuin4,Sirtuin5,Sirtuin6,Sirtuin7,pyroptosis”,最后纳入71篇文献进行综述。结果与结论:①沉默信息调节因子家族均参与了对细胞焦亡的调控;②过表达沉默信息调节因子1、沉默信息调节因子4可通过多种通路抑制细胞焦亡,从而缓解细胞焦亡对机体的损害;③沉默信息调节因子3除了影响细胞焦亡经典通路外,还能通过增强线粒体活性氧的清除能力、有丝分裂来抑制细胞焦亡;④沉默信息调节因子5参与细胞内代谢和能量平衡的调节,包括能量的摄入、储存和消耗;⑤沉默信息调节因子6既能通过多种通路影响细胞焦亡,还能影响巨噬细胞M1极化、活性氧的生成以及细胞焦亡相关因子消皮素D的裂解以抑制细胞焦亡;⑥过表达沉默信息调节因子7可抑制细胞焦亡;⑦沉默信息调节因子2与其他家族成员不同,其被敲降后才可抑制细胞焦亡,但报道较少,需要更为深入与全面的研究。展开更多
Trans-(-)-ε-viniferin(ε-viniferin)has antioxidative and anti-inflammatory effects.It also has neuroprotective effects in Huntington's disease by activating the SIRT3/LKB1/AMPK signaling pathway;however,it remain...Trans-(-)-ε-viniferin(ε-viniferin)has antioxidative and anti-inflammatory effects.It also has neuroprotective effects in Huntington's disease by activating the SIRT3/LKB1/AMPK signaling pathway;however,it remains unknown whetherε-viniferin also has a neuroprotective role in Parkinson's disease.A Parkinson's disease cell model was induced by exposing SH-SY5 Y cells to 3.0μM rotenone for 24 hours,and cells were then treated with 1.0μMε-viniferin for 24 hours.Treatment withε-viniferin upregulated SIRT3 expression,which promoted FOXO3 deacetylation and nuclear localization.ε-Viniferin also increased ATP production and decreased reactive oxygen species production.Furthermore,ε-viniferin treatment alleviated rotenone-induced mitochondrial depolarization and reduced cell apoptosis,and restored the expression of mitochondrial homeostasis-related proteins.However,when cells were transfected with SIRT3 or FOXO3 shRNA prior to rotenone andε-viniferin treatment,these changes were reversed.The results from the present study indicate thatε-viniferin enhances SIRT3-mediated FOXO3 deacetylation,reduces oxidative stress,and maintains mitochondrial homeostasis,thus inhibiting rotenone-induced cell apoptosis.ε-Viniferin may therefore be a promising treatment strategy for Parkinson's disease.展开更多
AIM: To explore the effects of IκBα SUMOylation and NF-κB p65 deacetylation on NF-κB p65 activity induced by high glucose in cultured human lens epithelial cells(HLECs).METHODS: HLECs(SRA01/04) were cultured with ...AIM: To explore the effects of IκBα SUMOylation and NF-κB p65 deacetylation on NF-κB p65 activity induced by high glucose in cultured human lens epithelial cells(HLECs).METHODS: HLECs(SRA01/04) were cultured with 5.5, 25, and 50 mmol/L glucose media for 24 h, and with 50 mmol/L glucose media for 0, 12, and 24 h respectively. SUMO1 and SIRT1 expressions were detected by reverse transcriptionpolymerase chain reaction(RT-PCR) and Western blot(WB). IκBα and NF-κB p65 expressions were detected by WB. With NAC, DTT, MG132 or Resveratrol(RSV) treatment, SUMO1 and SIRT1 expressions were detected by WB. Protein expression localizations were examined by immunofluorescence and co-immunofluorescence. The effects of SUMO1 or SIRT1 overexpression, as well as MG132 and RSV, on the nuclear expression and activity of IκBα and NF-κB p65 were analyzed by immunoblot and dual luciferase reporter gene assay.RESULTS: SUMO1 and SIRT1 expressions were influenced by high glucose in mRNA and protein levels, which could be blocked by NAC or DTT. SUMO1 was down-regulated by using MG132, and SIRT1 was up-regulated under RSV treatment. IκBα nuclear expression was attenuated and NF-κB p65 was opposite under high glucose, while IκBα and NF-κB p65 location was transferred to the nucleus. SUMO1 or SIRT1 overexpression and MG132 or RSV treatment affected the nuclear expression and activity of IκBα and NF-κB p65 under high glucose condition.CONCLUSION: IκBα SUMOylation and NF-κB p65 deacetylation affect NF-κB p65 activity in cultured HLECs under high glucose, and presumably play a significant role in controlling diabetic cataract.展开更多
Chitin and chitosan films were prepared by solution casting method. Chitosan specimens used in this study were deacetylated by 50.4%, 69.2%, 85.5% and 96.3%. Their water content, protein adhesion ability, cytocompatib...Chitin and chitosan films were prepared by solution casting method. Chitosan specimens used in this study were deacetylated by 50.4%, 69.2%, 85.5% and 96.3%. Their water content, protein adhesion ability, cytocompatibility, cell adhesion ability, in vitro and vivo degradability and biocompatibility were evaluated. Results indicated that with the degree of deacetylation （DD） between 50% and 70%, the chitosan showed higher water content. The higher the DD, the stronger protein adhesion ability the chitosan had. All the films have good cytocompatibility and the films with higher DD have better cell adhesion ability. Chitin films degraded more rapidly than others, which disappeared in 2 to 4 weeks after they were implanted in subcutaneous tissue and musculature. Their inflammatory reaction became weaker as the films degraded. As the DD got higher, the films degraded slower. The films of DD 85.5% and DD 90.3% even didn＇t disappeared in 12 weeks after they were implanted. Their inflammatory reaction was mild at the beginning of degradation, and became severe in 4 to 8 weeks, then weaken at last. This basic result can be very helpful for tissue engineering.展开更多
文摘背景:牙周炎是以牙菌斑生物膜为主要致病物质的炎症性、破坏性疾病,发生于牙龈、牙周膜、牙槽骨和牙骨质。细菌复合体的抗原及其分泌的毒素、酶等直接导致牙周组织的破坏,并引发宿主的免疫反应,使机体组织受到间接损害。沉默信息调节因子(Sirtuins,SIRTs)在抗衰老、抗氧化应激、调节炎症、介导细胞自噬等方面发挥重要作用,与牙周炎的发生和发展也有着密切的关系。目的:针对Sirtuins在牙周炎中的研究概况做一综述。方法:由第一作者应用计算机在PubMed、Web of Science、中国知网和万方数据库检索涉及Sirtuins在牙周炎中的相关研究,以“Sirtuins,Sirtuin1-7,periodontitis”为英文检索词,“沉默信息调节因子,沉默信息调节因子1-7,牙周炎”为中文检索词,经过筛选后纳入57篇文献进行综述分析。结果与结论:①SIRT1、SIRT2、SIRT3、SIRT6参与调控了牙周炎的发生与发展;②SIRT1:抑制SIRT1表达可能是牙周炎治疗靶点;SIRT1的过表达对牙周炎症有抑制作用,保护牙周组织;SIRT1的激活剂可减轻牙周组织的炎症,并可改善牙周炎引起的全身组织病变;③SIRT2:参与烟酰胺磷酸核糖转移酶介导的牙周炎症,SIRT2在牙周疾病的治疗和转归中发挥一定的作用;④SIRT3:可改善年龄相关的牙周病;天麻素可通过SIRT3的上调促进牙周膜干细胞成骨分化;SIRT3的激活剂通过调节细胞自噬水平,降低牙周炎对牙周和肾脏组织的破坏程度;⑤SIRT6:可抑制牙周组织炎症反应,抑制成牙骨质细胞的分化和矿化;SIRT6对根尖周炎的预后有利;⑥SIRT4、SIRT5、SIRT7与牙周炎的关系鲜有报道。
文摘背景:不同于非炎症性细胞凋亡,细胞焦亡是炎症性细胞死亡的一种形式,它伴随着膜完整性的破坏和促炎性细胞内物质的释放,因而与多种疾病有关。沉默信息调节因子家族是依赖于烟酰胺腺嘌呤二核苷酸的组蛋白去乙酰化酶家族。除了去乙酰化外,还具有其他酶活性,如脱琥珀酸化、脱丙酰化和腺苷二磷酸-核糖基化等,在参与细胞焦亡调控中发挥重要的作用。目的:综述沉默信息调节因子家族在细胞焦亡中的作用及影响。方法:第一作者通过检索PubMed、Web of Science、中国知网、万方数据库,检索时限为各数据库建库至2024年3月,中文检索词为“沉默信息调节因子,沉默信息调节因子1,沉默信息调节因子2,沉默信息调节因子3,沉默信息调节因子4,沉默信息调节因子5,沉默信息调节因子6,沉默信息调节因子7,细胞焦亡”,英文检索词为“Sirtuins,Sirtuin1,Sirtuin2,Sirtuin3,Sirtuin4,Sirtuin5,Sirtuin6,Sirtuin7,pyroptosis”,最后纳入71篇文献进行综述。结果与结论:①沉默信息调节因子家族均参与了对细胞焦亡的调控;②过表达沉默信息调节因子1、沉默信息调节因子4可通过多种通路抑制细胞焦亡,从而缓解细胞焦亡对机体的损害;③沉默信息调节因子3除了影响细胞焦亡经典通路外,还能通过增强线粒体活性氧的清除能力、有丝分裂来抑制细胞焦亡;④沉默信息调节因子5参与细胞内代谢和能量平衡的调节,包括能量的摄入、储存和消耗;⑤沉默信息调节因子6既能通过多种通路影响细胞焦亡,还能影响巨噬细胞M1极化、活性氧的生成以及细胞焦亡相关因子消皮素D的裂解以抑制细胞焦亡;⑥过表达沉默信息调节因子7可抑制细胞焦亡;⑦沉默信息调节因子2与其他家族成员不同,其被敲降后才可抑制细胞焦亡,但报道较少,需要更为深入与全面的研究。
基金supported by the National Natural Science Foundation of China,Nos.81771271(to JF),81801710(to YM)the Science and Technology Project Funds from Education Department of Liaoning Province of China,Nos.LK2016022(to SZ),LK2016021(to YM)。
文摘Trans-(-)-ε-viniferin(ε-viniferin)has antioxidative and anti-inflammatory effects.It also has neuroprotective effects in Huntington's disease by activating the SIRT3/LKB1/AMPK signaling pathway;however,it remains unknown whetherε-viniferin also has a neuroprotective role in Parkinson's disease.A Parkinson's disease cell model was induced by exposing SH-SY5 Y cells to 3.0μM rotenone for 24 hours,and cells were then treated with 1.0μMε-viniferin for 24 hours.Treatment withε-viniferin upregulated SIRT3 expression,which promoted FOXO3 deacetylation and nuclear localization.ε-Viniferin also increased ATP production and decreased reactive oxygen species production.Furthermore,ε-viniferin treatment alleviated rotenone-induced mitochondrial depolarization and reduced cell apoptosis,and restored the expression of mitochondrial homeostasis-related proteins.However,when cells were transfected with SIRT3 or FOXO3 shRNA prior to rotenone andε-viniferin treatment,these changes were reversed.The results from the present study indicate thatε-viniferin enhances SIRT3-mediated FOXO3 deacetylation,reduces oxidative stress,and maintains mitochondrial homeostasis,thus inhibiting rotenone-induced cell apoptosis.ε-Viniferin may therefore be a promising treatment strategy for Parkinson's disease.
基金Supported by the National Natural Science Foundation of China(No.81170836 No.81570838)
文摘AIM: To explore the effects of IκBα SUMOylation and NF-κB p65 deacetylation on NF-κB p65 activity induced by high glucose in cultured human lens epithelial cells(HLECs).METHODS: HLECs(SRA01/04) were cultured with 5.5, 25, and 50 mmol/L glucose media for 24 h, and with 50 mmol/L glucose media for 0, 12, and 24 h respectively. SUMO1 and SIRT1 expressions were detected by reverse transcriptionpolymerase chain reaction(RT-PCR) and Western blot(WB). IκBα and NF-κB p65 expressions were detected by WB. With NAC, DTT, MG132 or Resveratrol(RSV) treatment, SUMO1 and SIRT1 expressions were detected by WB. Protein expression localizations were examined by immunofluorescence and co-immunofluorescence. The effects of SUMO1 or SIRT1 overexpression, as well as MG132 and RSV, on the nuclear expression and activity of IκBα and NF-κB p65 were analyzed by immunoblot and dual luciferase reporter gene assay.RESULTS: SUMO1 and SIRT1 expressions were influenced by high glucose in mRNA and protein levels, which could be blocked by NAC or DTT. SUMO1 was down-regulated by using MG132, and SIRT1 was up-regulated under RSV treatment. IκBα nuclear expression was attenuated and NF-κB p65 was opposite under high glucose, while IκBα and NF-κB p65 location was transferred to the nucleus. SUMO1 or SIRT1 overexpression and MG132 or RSV treatment affected the nuclear expression and activity of IκBα and NF-κB p65 under high glucose condition.CONCLUSION: IκBα SUMOylation and NF-κB p65 deacetylation affect NF-κB p65 activity in cultured HLECs under high glucose, and presumably play a significant role in controlling diabetic cataract.
基金the China"863"High-technology Development Program under contract No.2003AA625050.
文摘Chitin and chitosan films were prepared by solution casting method. Chitosan specimens used in this study were deacetylated by 50.4%, 69.2%, 85.5% and 96.3%. Their water content, protein adhesion ability, cytocompatibility, cell adhesion ability, in vitro and vivo degradability and biocompatibility were evaluated. Results indicated that with the degree of deacetylation （DD） between 50% and 70%, the chitosan showed higher water content. The higher the DD, the stronger protein adhesion ability the chitosan had. All the films have good cytocompatibility and the films with higher DD have better cell adhesion ability. Chitin films degraded more rapidly than others, which disappeared in 2 to 4 weeks after they were implanted in subcutaneous tissue and musculature. Their inflammatory reaction became weaker as the films degraded. As the DD got higher, the films degraded slower. The films of DD 85.5% and DD 90.3% even didn＇t disappeared in 12 weeks after they were implanted. Their inflammatory reaction was mild at the beginning of degradation, and became severe in 4 to 8 weeks, then weaken at last. This basic result can be very helpful for tissue engineering.
