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    Hydroxytyrosol prevents periodontitis-induced bone loss by regulating mitochondrial function and mitogen-activated protein kinase signaling of bone cells. Zhang Xiaorong,Jiang Yun,Mao Jiajie,Ren Xuekun,Ji Yinghui,Mao Yixin,Chen Yang,Sun Xiaoyu,Pan Yihuai,Ma Jianfeng,Huang Shengbin Free radical biology & medicine Reactive oxygen species (ROS) overproduction promotes the alveolar bone loss during the development of periodontitis. Mitochondria are the principal source of ROS. Hydroxytyrosol (HT), a natural phenolic compound present in olive oil, is well known for its antioxidant and mitochondrial-protective prosperities. Nonetheless, the impact of HT on periodontitis and its related mechanisms underlying bone cell behavior remains unknown. Osteoclasts differentiated from RAW264.7 model and oxidative stress (OS) induced pre-osteoblast MC3T3-E1 cell injury model were treated with and without HT. Cell viability, apoptosis, differentiation, mitochondrial function along with mitogen-activated protein kinase (MAPK) signaling pathway were investigated. Meanwhile, the effect and related mechanisms of HT on bone loss in mice with periodontitis were also detected. HT inhibited osteoclast differentiation and prevented OS induced pre-osteoblast cells injury via regulating mitochondrial function as well as ERK and JNK signaling pathways. Moreover, HT attenuated the alveolar bone loss, increased bone forming activity, inhibited the osteoclasts differentiation and decreased the level of OS in mice with periodontitis. Our findings, for the first time, revealed a novel function of HT in bone remodeling of periodontitis, and highlighted its therapeutical potential for the prevention/treatment of periodontitis. 10.1016/j.freeradbiomed.2021.09.027
    Mitochondrial DNA Efflux Maintained in Gingival Fibroblasts of Patients with Periodontitis through ROS/mPTP Pathway. Oxidative medicine and cellular longevity Mitochondria have their own mitochondrial DNA (mtDNA). Aberrant mtDNA is associated with inflammatory diseases. mtDNA is believed to induce inflammation via the abnormal mtDNA release. Periodontitis is an infectious, oral inflammatory disease. Human gingival fibroblasts (HGFs) from patients with chronic periodontitis (CP) have shown to generate higher reactive oxygen species (ROS) that cause oxidative stress and have decreased mtDNA copy number. Firstly, cell-free mtDNA was identified in plasma from CP mice through qRT-PCR. Next, we investigated whether mtDNA efflux was maintained in primary cultures of HGFs from CP patients and the possible underlying mechanisms using adenovirus-mediated transduction live cell imaging and qRT-PCR analysis. Here, we reported that mtDNA was increased in plasma from the CP mice. Additionally, we confirmed that CP HGFs had significant mtDNA efflux from mitochondria compared with healthy HGFs. Furthermore, lipopolysaccharide (LPS) from can also cause mtDNA release in healthy HGFs. Mechanistically, LPS upregulated ROS levels and mitochondrial permeability transition pore (mPTP) opening by inhibition of pyruvate dehydrogenase kinase (PDK)2 expression, resulting in mtDNA release. Importantly, mtDNA efflux was even persistent in HGFs after LPS was removed and cells were passaged to the next three generations, indicating that mtDNA abnormalities were retained in HGFs in vitro, similar to the primary hosts. Taken together, our results elucidate that mtDNA efflux was maintained in HGFs from periodontitis patients through abnormal ROS/mPTP activity. Therefore, our work indicates that persistent mtDNA efflux may be a possible diagnostic and therapeutic target for patients with periodontitis. 10.1155/2022/1000213
    Mitochondrial abnormalities are involved in periodontal ligament fibroblast apoptosis induced by oxidative stress. Chen Yuting,Ji Yinghui,Jin Xing,Sun Xiaoyu,Zhang Xiaorong,Chen Yang,Shi Lixi,Cheng Haoran,Mao Yixin,Li Xumin,Hou Yubo,Zhang Dafeng,Zhao Shufan,Ma Jianfeng,Huang Shengbin Biochemical and biophysical research communications Oxidative stress (OS)-induced apoptosis of periodontal ligament cells (PDLCs) has been suggested to be an important pathogenic factor of periodontitis. Mitochondrial abnormalities are closely linked to OS and act as the main players in apoptosis. Our aim was to investigate the potential mitochondrial abnormalities in PDLCs apoptosis induced by OS. In this study, significant reduction in viability and increased apoptosis were observed in HO-treated hPDLCs. HO also induced mitochondrial dysfunction, judging by increased mitochondrial reactive oxygen species amounts, and decreased mitochondrial membrane potential as well as ATP levels. Furthermore, HO significantly enhanced mitochondrial fission by decreasing the expression of Mfn1 and Mfn2, along with increasing the expression of Drp1, Fis1 and the cleavage of OPA1. Notably, NAC stabilized the balance of the mitochondrial dynamics, attenuated mitochondrial dysfunction, and inhibited apoptosis of hPDLCs in the presence of HO. In conclusion, the OS-induced apoptosis of hPDLCs may be mediated by mitochondria-dependent pathway. 10.1016/j.bbrc.2018.12.143
    Mitochondrial dysfunction is involved in the aggravation of periodontitis by diabetes. Sun Xiaoyu,Mao Yixin,Dai Panpan,Li Xumin,Gu Weiyan,Wang Huining,Wu Gang,Ma Jianfeng,Huang Shengbin Journal of clinical periodontology AIM:To elucidate whether mitochondrial dysfunction contributes to aggravated periodontitis in diabetes. MATERIALS AND METHODS:Sixty-four wistar rats were randomly assigned into four groups: control, periodontitis, diabetes, and diabetic periodontitis. Two weeks after induction of diabetes, periodontitis was induced by silk ligation for 2 weeks and thereafter evaluated by assessing alveolar bone loss and apoptosis of periodontium cells. Mitochondrial oxidative stress was detected by MitoSOX staining. Mitochondrial function was determined by measuring ATP production, and by assessing mitochondrial DNA copy number, activities of electron transport chain complexes, and biogenesis with real-time PCR. RESULTS:Significantly severer bone loss, enhanced periodontium cell apoptosis, and mitochondrial oxidative stress were found in the rats with diabetic periodontitis than the others. Furthermore, diabetic rats with periodontitis presented severer mitochondrial dysfunction than lean rats with periodontitis, as reflected by compromised ATP production, decreased mitochondrial DNA copy number, reduced gene expression of electron transport chain complex I subunits, and impaired mitochondrial biogenesis (p < 0.05). Multiple regression analysis further indicated a close correlation between these mitochondrial events and bone loss in diabetic periodontitis. CONCLUSIONS:Mitochondrial dysfunction was positive correlated to aggravated periodontitis in diabetes and might represent a therapeutic target for diabetic periodontitis. 10.1111/jcpe.12711
    Resveratrol protects renal damages induced by periodontitis via preventing mitochondrial dysfunction in rats. Li Xin,Liu Xin-Chan,Ding Xu,Liu Xiao-Meng,Cao Niu-Ben,Deng Yu,Hou Yu-Bo,Yu Wei-Xian Oral diseases OBJECTIVES:Periodontitis is closely associated with kidney disease and reactive oxygen species (ROS) involvement. Mitochondria are the primary source of both endogenous ROS and renal energy. We investigated whether resveratrol (RSV) prevents renal injury and mitochondrial dysfunction in periodontitis rats. METHODS:Thirty male Wistar rats were divided into control, experimental periodontitis (Ep) and Ep-RSV groups. To induce periodontitis, a steel ligature was placed on the cervix of the bilateral first maxillary molars. RSV (50 mg/kg/day) to the Ep-RSV group and vehicle to the Ep and control groups were gavaged. After 8 weeks, alveolar bone loss, pocket depth, gingival blood index and tooth mobility were assessed. Oxidative stress parameters, mitochondrial structure, mitochondrial membrane potential (MMP), mitochondrial ROS, adenosine triphosphate (ATP), sirtuin 1 (SIRT1) and peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) were analysed in renal. Renal function and histology were also evaluated. RESULTS:Compared with the control group, the Ep group showed renal structural destruction, elevated oxidative stress levels, mitochondrial structure destruction, MMP loss, mitochondrial ROS accumulation, ATP reduction, and decreased SIRT1 and PGC-1α levels. RSV prevented these destruction (p < 0.05). However, there was no significant impairment in renal function (p > 0.05). CONCLUSIONS:Periodontitis induces mitochondrial dysfunction in renal tissues. Resveratrol exerts a preventive effect on periodontitis-induced kidney injury by preventing mitochondrial dysfunction. 10.1111/odi.14148
    Mitochondrial polymorphisms and dysfunction related to aggressive periodontitis: a pilot study. Wang X,Luan Q,Chen Q,Zhao L,Guo Y Oral diseases AIM:To investigate whether aggressive periodontitis (AgP) is associated with specific mtDNA polymorphisms or point mutations and furthermore whether mitochondrial dysfunction occurs in gingival fibroblasts of AgP patients. MATERIALS AND METHODS:The mitochondrial DNA coding regions were amplified and sequenced in 22 overlapped fragments in 34 patients with AgP and 28 healthy controls for initial screening. We selected eleven SNPs for detailed investigation in the rest 30 AgP patients and 26 healthy controls, because all other variants occurred at relatively low frequencies or had no difference between two groups. Logistic regression models were used to analyze the association between mtDNA variants and AgP. Gingival fibroblasts were cultured from four patients with AgP and four healthy controls, and then mitochondrial membrane potential, reactive oxygen species production and cell proliferation were analyzed. RESULTS:Significant association was observed between aggressive periodontitis and eight mitochondrial polymorphisms: '8701A-9540T-10400C-10873T-14783T-15043G-15301G' (OR = 3.471 (1.610-7.483), P = 0.001) and 10398A (OR = 3.238 (1.481-7.078), P = 0.003). Compared with the controls, patients with aggressive periodontitis had a decrease in mitochondrial membrane potential and an increase in reactive oxygen species production. CONCLUSION:In conclusion, we propose that mitochondrial dysfunction and '8701A-9540T-10400C-10873T-14783T-15043G-15301G, 10398A' are associated with and may increase the susceptibility to AgP in the Han Chinese population. 10.1111/odi.12163
    Mitochondrial dysfunction and genetic heterogeneity in chronic periodontitis. Govindaraj Periyasamy,Khan Nahid Akhtar,Gopalakrishna Praturi,Chandra Rampalli Viswa,Vanniarajan Ayyasamy,Reddy Aileni Amarendra,Singh Shashi,Kumaresan Rathinam,Srinivas Gunda,Singh Lalji,Thangaraj Kumarasamy Mitochondrion We performed an extensive study on mitochondrial dysfunction in chronic periodontitis (CP). Electron microscopic analysis of gingival cells revealed abnormal mitochondria in 60% of the patients. Mitochondrial membrane potential and oxygen consumption of gingival cells were reduced by 4 fold and 5.8 fold, respectively; whereas ROS production was increased by 18%. The genetic analysis by complete mitochondrial DNA sequencing revealed the identification of 14 novel mutations only in periodontal tissues but not in the blood, suggesting a role of oxidative stress on periodontal tissues. Thus, our functional and genetic analysis provided an evidence for the mitochondrial dysfunction in CP. 10.1016/j.mito.2011.01.009
    Periodontitis and cognitive impairment in older adults: The mediating role of mitochondrial dysfunction. Journal of periodontology BACKGROUND:Increased attention has been focused on the associations of periodontal disease with the onset and progression of cognitive impairment. Although the associations are likely to be multifactorial, few studies have explored the role of mitochondrial dysfunction in the periodontitis-dementia link. METHODS:Cross-sectional data of 1,883 participants aged ≥60 years in the National Health and Nutrition Examination Survey 2011-2014 were analyzed. The following data were collected: 1) general information on sociodemographic, behavioral, and health-related factors; 2) periodontal status (mean attachment loss [AL] and mean probing depth [PD]); 3) mitochondrion-derived biomarker of mitochondrial dysfunction (blood sample concentration of methylmalonic acid [MMA]); 4) cognitive function (Consortium to Establish a Registry for Alzheimer's disease immediate recall [CERAD-IR] and delay recall [CERAD-DR], animal fluency test, and digit symbol substitution test [DSST]). Mediation analysis weighted for complex survey design was used to assess the effect of MMA on the association of periodontal status with cognitive function after adjusting for potential confounders. RESULTS:Participants with Stage III and IV periodontitis had lower scores on cognitive performance and higher MMA levels than those with Stages I/II periodontitis. Circulating MMA was significantly associated with CERAD-DR (weighted β [SE] = -0.076 [0.011]) and DSST (weighted β [SE] = -0.039 [0.009]), which mediated 9.9% and 6.0% of the total association of mean PD with cognitive function. Moreover, MMA mediated 11.7% and 5.8% of the association of mean AL with CERAD-DR and DSST, respectively. CONCLUSION:The findings suggest that MMA, a biomarker of mitochondrial dysfunction, plays a mediating role in the link between periodontitis and cognitive impairment in older adults aged ≥60 years. 10.1002/JPER.21-0620