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1.
Qing-Qiu Mao Xiao-Ming Zhong Chun-Rong Feng Ai-Juan Pan Zhao-Yi Li Zhen Huang 《Cellular and molecular neurobiology》2010,30(7):1059-1066
Preclinical and clinical investigations have shown hippocampal neuronal atrophy and destruction were observed in patients
with depression, which could be ameliorated by the treatment with antidepressants. Therefore, neuroprotection has been proposed
to be one of the acting mechanisms of antidepressant. Paeoniflorin, a monoterpene glycoside, has been reported to display
antidepressant-like effects in animal models of behavioral despair. The present study aimed to examine the protective effect
of paeoniflorin on glutamate-induced neurotoxicity in cultured rat pheochromocytoma (PC12) cells. The results showed that
pretreatment with paeoniflorin elevated cell viability, inhibited apoptosis, decreased levels of intracellular reactive oxygen
species and malondialdehyde, and enhanced activity of superoxide dismutase in glutamate-treated PC12 cells. Pretreatment with
paeoniflorin also reversed the increased intracellular Ca2+ concentration and the reduced Calbindin-D28K mRNA level caused by glutamate in PC12 cells. The results suggest that paeoniflorin
exerts a neuroprotective effect on glutamate-induced neurotoxicity in PC12 cells, at least in part, via inhibiting oxidative
stress and Ca2+ overload. This neuroprotective effect may be one of the action pathways accounting for the in vivo antidepressant activity
of paeoniflorin. 相似文献
2.
Hyperactivation of the hypothalamic–pituitary–adrenal axis and the associated hippocampal atrophy were observed in patients
with depression, which could be ameliorated by the treatment with antidepressants. Therefore, neuroprotection has been proposed
to be one of the acting mechanisms of antidepressant. Our previous studies have showed that treating mice with piperine produced
antidepressant-like effect in animal models of behavioral despair. This study aimed to examine the protective effect of piperine
treatment on corticosterone-induced neurotoxicity in cultured rat pheochromocytoma (PC12) cells. The results showed that piperine
co-treatment revealed a differential effect on the cytotoxicity of corticosterone and had its maximum inhibitory effect at
1 μM. Piperine (1 μM) co-treatment also significantly decreased intracellular reactive oxygen species level, and enhanced
superoxide dismutase activity and total glutathione level in corticosterone-treated PC12 cells. In addition, piperine (1 μM)
co-treatment was found to reverse the decreased brain-derived neurotrophic factor (BDNF) mRNA level caused by corticosterone
in PC12 cells. The results suggest that piperine exerts a neuroprotective effect on corticosterone-induced neurotoxicity in
PC12 cells, at least in part, via the inhibition of oxidative stress and the upregulation of BDNF mRNA expression. This neuroprotective
effect may be one of the acting mechanisms accounts for the in vivo antidepressant activity of piperine. 相似文献
3.
Background
This paper describes a microarray study including data quality control, data analysis and the analysis of the mechanism of toxicity (MOT) induced by 1-methyl-4-phenylpyridinium (MPP+) in a rat adrenal pheochromocytoma cell line (PC12 cells) using bioinformatics tools. MPP+ depletes dopamine content and elicits cell death in PC12 cells. However, the mechanism of MPP+-induced neurotoxicity is still unclear.Results
In this study, Agilent rat oligo 22K microarrays were used to examine alterations in gene expression of PC12 cells after 500 μM MPP+ treatment. Relative gene expression of control and treated cells represented by spot intensities on the array chips was analyzed using bioinformatics tools. Raw data from each array were input into the NCTR ArrayTrack database, and normalized using a Lowess normalization method. Data quality was monitored in ArrayTrack. The means of the averaged log ratio of the paired samples were used to identify the fold changes of gene expression in PC12 cells after MPP+ treatment. Our data showed that 106 genes and ESTs (Expressed Sequence Tags) were changed 2-fold and above with MPP+ treatment; among these, 75 genes had gene symbols and 59 genes had known functions according to the Agilent gene Refguide and ArrayTrack-linked gene library. The mechanism of MPP+-induced toxicity in PC12 cells was analyzed based on their genes functions, biological process, pathways and previous published literatures.Conclusion
Multiple pathways were suggested to be involved in the mechanism of MPP+-induced toxicity, including oxidative stress, DNA and protein damage, cell cycling arrest, and apoptosis.4.
Julie Bournival Patrik Quessy Maria-Grazia Martinoli 《Cellular and molecular neurobiology》2009,29(8):1169-1180
Reactive oxygen species produced by oxidative stress may participate in the apoptotic death of dopamine neurons distinctive
of Parkinson’s disease. Resveratrol, a red wine extract, and quercetin, found mainly in green tea, are two natural polyphenols,
presenting antioxidant properties in a variety of cellular paradigms. The aim of this study was to evaluate the effect of
resveratrol and quercetin on the apoptotic cascade induced by the administration of 1-methyl-4-phenylpyridinium ion (MPP+), a Parkinsonian toxin, provoking the selective degeneration of dopaminergic neurons. Our results show that a pre-treatment
for 3 h with resveratrol or quercetin before MPP+ administration could greatly reduce apoptotic neuronal PC12 death induced by MPP+. We also demonstrated that resveratrol or quercetin modulates mRNA levels and protein expression of Bax, a pro-apoptotic
gene, and Bcl-2, an anti-apoptotic gene. We then evaluated the release of cytochrome c and the nuclear translocation of the apoptosis-inducing factor (AIF). Altogether, our results indicate that resveratrol and
quercetin diminish apoptotic neuronal cell death by acting on the expression of pro- and anti-apoptotic genes. These findings
support the role of these natural polyphenols in preventive and/or complementary therapies for several human neurodegenerative
diseases caused by oxidative stress and apoptosis. 相似文献
5.
The present study aimed to examine the protective effect of ginsenoside Rg1 against colistin-induced neurotoxicity in cultured rat pheochromocytoma (PC12) cells. Ginsenoside Rg1 was shown to elevate cell viability, decrease levels of malondialdehyde and intracellular reactive oxygen species, enhance activity of superoxide dismutase and glutathione, and decrease the release of cytochrome-c, formation of DNA fragmentation in colistin-treated PC12 cells. Ginsenoside Rg1 also reversed the increased caspase-9 and -3 mRNA levels caused by colistin in PC12 cells. These results suggest that ginsenoside Rg1 exerts a neuroprotective effect on colistin-induced neurotoxicity in PC12 cells, at least in part, via the inhibition of oxidative stress, prevention of apoptosis mediated via mitochondria pathway. Co-administration of ginsenoside Rg1 highlights the potential to increase the therapeutic index of colistin. 相似文献
6.
7.
The neurotoxin 1-methy-4-phenylpyridinium (MPP+) is used for its’ capacity to induce Parkinsonism through its inhibitory effects on mitochondrial complex I. This inhibition
disrupts cellular energy formation and aerobic glycolysis. The objective of this study was to demonstrate that the toxic effect
of mitochondrial aerobic pathway inhibition with MPP+ can be reduced by stimulating anaerobic glycolysis using glucose supplementation. In this study, C6 Glioma cell viability
was examined in the presence of different concentrations of MPP alone and with the addition of glucose. The results obtained
indicate that there was a significant increase (P < 0.001) in cell viability in cells treated with glucose and MPP+ verses cells treated with MPP+ alone. Fluorometric analysis using 100 uM Rhodamine 123 indicated mitochondrial membrane potential was not restored in MPP+ treated cells with glucose; however, normal cell viability was confirmed using 2 ug/ml Fluorescein diacetate. This dual fluorescence
indicated mitochondrial damage from MPP+ while glucose augmented cell survival. Further confirmation of cell survival upon damage to the mitochondria was evident in
TUNEL staining. Positive staining was prominent only in MPP+ treatment groups alone, while control and co-treated groups exhibited little to no TUNEL staining. ATP measurements of all
MPP+ treated groups exhibited a significant (P < 0.001) decrease verses control. Groups co-treated with MPP+ and glucose revealed a significant increase (250 μM group: P < 0.001) in ATP. It was concluded from this study that glucose supplementation was able to sustain cellular viability and
ATP production through anaerobic glycolysis despite the inhibitory effect of MPP+ on aerobic glycolysis. 相似文献
8.
9.
Ramesh B. Badisa Selina F. Darling-Reed Karam F. A. Soliman 《Neurochemical research》2010,35(9):1413-1421
Impaired mitochondrial function in glial and neuronal cells in the substantia nigra is one of the most likely causes of Parkinson’s
disease. In this study, we investigated the protective role of glucose on early key events associated with MPP+-induced changes in rat C6 astroglial cells. Studies were carried out to examine alterations in mitochondrial respiratory
status, membrane potential, glutathione levels, and cell cycle phase inhibition at 48 h in 2 and 10 mM glucose in media. The
results obtained suggest that MPP+ caused significant cell death in 2 mM glucose with LC50 0.14 ± 0.005 mM, while 10 mM glucose showed highly significant protection against MPP+ toxicity with LC50 0.835 ± 0.03 mM. This protection was not observed with cocaine, demonstrating its compound specificity. MPP+ in 2 mM glucose decreased significantly mitochondrial respiration, membrane potential and glutathione levels in a dose dependent
manner, while 10 mM glucose significantly restored them. MPP+ in 2 mM glucose arrested the cells at G0/G1 and G2/M phases, demonstrating its dual inhibitory effects. However, in 10 mM
glucose, MPP+ caused G0/G1 arrest only. In summary, the results suggest that loss of cell viability in 2 mM glucose group with MPP+ treatments was due to mitochondrial dysfunction caused by multilevel mechanism, involving significant decrease in mitochondrial
respiration, membrane potential, glutathione levels, and dual arrest of cell phases, while 10 mM glucose rescued astroglial
cells from MPP+ toxicity by significant maintenance of these factors. 相似文献
10.
A-Rang Im Young-Hwa Kim Md. Romij Uddin Sungwook Chae Hye Won Lee Yun Hee Kim Yeong Shik Kim Mi-Young Lee 《Cellular and molecular neurobiology》2013,33(5):625-635
Rotenone is an inhibitor of mitochondrial complex I-induced neurotoxicity in PC12 cells and has been widely studied to elucidate the pathogenesis of Parkinson’s disease. We investigated the neuroprotective effects of betaine on rotenone-induced neurotoxicity in PC12 cells. Betaine inhibited rotenone-induced apoptosis in a dose-dependent manner, with cell viability increasing from 50 % with rotenone treatment alone to 71 % with rotenone plus 100-μM betaine treatment. Flow cytometric analysis demonstrated cell death in the rotenone-treated cells to be over 50 %; the number of live cells increased with betaine pretreatment. Betaine pretreatment of PC12 cells attenuated rotenone-mediated mitochondrial dysfunction, including nuclear fragmentation, ATP depletion, mitochondrial membrane depolarization, caspase-3/7 activation, and reactive oxygen species production. Western blots demonstrated activation of caspase-3 and caspase-9, and their increased expression levels in rotenone-treated cells; betaine decreased caspase-3 and caspase-9 expression levels and suppressed their activation. Together, these results suggest that betaine may serve as a neuroprotective agent in the treatment of neurodegenerative diseases. 相似文献
11.
Duraisamy Kempuraj Ramasamy Thangavel Ranan Fattal Sagar Pattani Evert Yang Smita Zaheer Donna A. Santillan Mark K. Santillan Asgar Zaheer 《Neurochemical research》2016,41(5):1042-1049
Microglial activation and release of inflammatory cytokines and chemokines are crucial events in neuroinflammation. Microglial cells interact and respond to other inflammatory cells such as T cells and mast cells as well as inflammatory mediators secreted from these cells. Recent studies have shown that neuroinflammation causes and accelerates neurodegenerative disease such as Parkinson’s disease (PD) pathogenesis. 1-methyl-4-phenyl-pyridinium ion (MPP+), the active metabolite of neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydro pyridine activates glial cells and mediate neurodegeneration through release of inflammatory mediators. We have shown that glia maturation factor (GMF) activates glia and induces neuroinflammation and neurodegeneration and that MPP+ activates mast cells and release proinflammatory cytokines and chemokines. The chemokine (C-C motif) ligand 2 (CCL2) levels have been shown to be elevated and play a role in PD pathogenesis. In the present study, we analyzed if MPP+ activates mouse and human mast cells to release chemokine CCL2. Mouse bone marrow-derived mast cells (BMMCs) and human umbilical cord blood-derived cultured mast cells (hCBMCs) were incubated with MPP+ (10 µM) for 24 h and CCL2 levels were measured in the supernatant media by ELISA. MPP+-significantly induced CCL2 release from BMMCs and hCBMCs. Additionally, GMF overexpression in BMMCs obtained from wild-type mice released significantly more CCL2, while BMMCs obtained from GMF-deficient mice showed less CCL2 release. Further, we show that MPP+-induced CCL2 release was greater in BMMCs–astrocyte co-culture conditions. Uncoupling protein 4 (UCP4) which is implicated in neurodegenerative diseases including PD was detected in BMMCs by immunocytochemistry. Our results suggest that mast cells may play role in PD pathogenesis. 相似文献
12.
CD4+CD25+Foxp3+ regulatory T (Treg) cells are believed to play an important role in suppressing autoimmunity and maintaining peripheral tolerance. How their survival is regulated in the periphery is less clear. Here we show that Treg cells express receptors for gamma chain cytokines and are dependent on an exogenous supply of these cytokines to overcome cytokine withdrawal apoptosis in vitro. This result was validated in vivo by the accumulation of Treg cells in Bim-/- and Bcl-2 tg mice which have arrested cytokine deprivation apoptosis. We also found that CD25 and Foxp3 expression were down-regulated in the absence of these cytokines. CD25+ cells from Scurfy mice do not depend on cytokines for survival demonstrating that Foxp3 increases their dependence on cytokines by suppressing cytokine production in Treg cells. Our study reveals that the survival of Treg cells is strictly dependent on cytokines and cytokine producing cells because they do not produce cytokines. Our study thus, demonstrates that different gamma chain cytokines regulate Treg homeostasis in the periphery by differentially regulating survival and proliferation. These findings may shed light on ways to manipulate Treg cells that could be utilized for their therapeutic applications. 相似文献
13.
Haruo Homareda Masahiro Otsu Sachiko Yamamoto Makoto Ushimaru Sayaka Ito Toshiyuki Fukutomi Taeho Jo Yoshinobu Eishi Yukichi Hara 《Journal of bioenergetics and biomembranes》2017,49(6):463-472
The affinity for K+ of silkworm nerve Na+/K+-ATPase is markedly lower than that of mammalian Na+/K+-ATPase (Homareda 2010). In order to obtain clues on the molecular basis of the difference in K+ affinities, we cloned cDNAs of silkworm (Bombyx mori) nerve Na+/K+-ATPase α and β subunits, and analyzed the deduced amino acid sequences. The molecular masses of the α and β subunits were presumed to be 111.5 kDa with ten transmembrane segments and 37.7 kDa with a single transmembrane segment, respectively. The α subunit showed 75% identity and 93% homology with the pig Na+/K+-ATPase α1 subunit. On the other hand, the amino acid identity of the β subunit with mammalian counterparts was as low as 30%. Cloned α and β cDNAs were co-expressed in cultured silkworm ovary-derived cells, BM-N cells, which lack endogenous Na+/K+-ATPase. Na+/K+-ATPase expressed in the cultured cells showed a low affinity for K+ and a high affinity for Na+, characteristic of the silkworm nerve Na+/K+-ATPase. These results suggest that the β subunit is responsible for the affinity for K+ of Na+/K+-ATPase. 相似文献
14.
A. M. Tverskoi S. V. Sidorenko E. A. Klimanova O. A. Akimova L. V. Smolyaninova O. D. Lopina S. N. Orlov 《Biochemistry. Biokhimii?a》2016,81(8):876-883
Side-by-side with inhibition of the Na+,K+-ATPase ouabain and other cardiotonic steroids (CTS) can affect cell functions by mechanisms other than regulation of the intracellular Na+ and K+ ratio ([Na+]i/[K+]i). Thus, we compared the doseand time-dependences of the effect of ouabain on intracellular [Na+]i/[K+]i ratio, Na+,K+-ATPase activity, and proliferation of human umbilical vein endothelial cells (HUVEC). Treatment of the cells with 1-3 nM ouabain for 24-72 h decreased the [Na+]i/[K+]i ratio and increased cell proliferation by 20-50%. We discovered that the same ouabain concentrations increased Na+,K+-ATPase activity by 25-30%, as measured by the rate of 86Rb+ influx. Higher ouabain concentrations inhibited Na+,K+-ATPase, increased [Na+]i/[K+]i ratio, suppressed cell growth, and caused cell death. When cells were treated with low ouabain concentrations for 48 or 72 h, a negative correlation between [Na+]i/[K+]i ratio and cell growth activation was observed. In cells treated with high ouabain concentrations for 24 h, the [Na+]i/[K+]i ratio correlated positively with proliferation inhibition. These data demonstrate that inhibition of HUVEC proliferation at high CTS concentrations correlates with dissipation of the Na+ and K+ concentration gradients, whereas cell growth stimulation by low CTS doses results from activation of Na+,K+-ATPase and decrease in the [Na+]i/[K+]i ratio. 相似文献
15.
Qing-Qiu Mao Siu-Po Ip Kam-Ming Ko Sam-Hip Tsai Ming Zhao Chun-Tao Che 《Cellular and molecular neurobiology》2009,29(5):643-647
Preclinical and clinical investigations have shown the involvement of dysregulation of hypothalamic–pituitary–adrenal (HPA)
axis in the pathogenesis of depression. Hypercortisolemia and the associated hippocampal atrophy were observed in patients
with depression, which could be ameliorated by the treatment with antidepressants. Therefore, neuroprotection has been proposed
to be one of the acting mechanisms of antidepressant. Previous studies in our laboratory have demonstrated the antidepressant-like
activity of total glycosides of peony (TGP) in mice. This study aimed to examine the effect of TGP treatment on corticosterone-induced
neurotoxicity in cultured rat pheochromocytoma (PC12) cells. Treating the cells with corticosterone at 200 μM for 48 h caused
apoptotic cell death. The cytotoxicity was associated with the activation of caspase-3 activity and the decrease in the mRNA
ratio of bcl-2 to bax. TPG treatment at increasing doses (1–10 mg/l) protected against the corticosterone-induced toxicity
in PC12 cells in a dose-dependent manner. The cytoprotection afforded by TGP treatment was associated with the inhibition
of caspase-3 activity and the up-regulation of bcl-2/bax mRNA ratio. The anti-apoptotic effect of TGP is therefore likely
mediated by the suppression of the mitochondrial pathway leading to apoptosis. 相似文献
16.
The aims of the present study were twofold: (1) simultaneous determinations of Na(+) transport parameters of erythrocytes from 40 healthy donors and 28 septic patients as assessed by a score of severity of sepsis (SSS), and (2) examination of the correlation between the SSS and specific Na(+) transport abnormalities. Erythrocytes were obtained and loaded with different ionic compositions and cellular Na(+) contents before determination of the near-maximal Na(+) pump rate (Vmax), the physiological extrusion rate of Na(+) (v) and the number of ouabain-binding sites (Bmax). In erythrocytes from septic patients, the cellular Na(+) content was 28% higher (p < 0.001), with no differences in water content compared to erythrocytes from healthy donors. This elevated Na(+) content was accompanied by significantly higher values for Vmax (43%), v (24%) and Bmax (48%) of the Na(+) pump in septic erythrocytes. Moreover, significant positive correlations existed between Vmax and SSS (p = 0.028) and between cellular Na(+) content and SSS (p = 0.005). These data suggest that during sepsis, membrane alterations occur and result in an increased cellular Na(+) content. Active Na(+) transport (Vmax and v) was significantly stimulated, possibly as a consequence of a secondary response to the elevated Na(+) of cells. Both cellular Na(+) and Vmax correlated well with the severity of sepsis, suggesting that these altered transport parameters may reflect the progress of sepsis. 相似文献
17.
The effect of ANG II on pHi, [Ca2+]i and cell volume was investigated in T84 cells, a cell line originated from colon epithelium, using the probes BCECF-AM, Fluo
4-AM and acridine orange, respectively. The recovery rate of pHi via the Na+/H+ exchanger was examined in the first 2 min following the acidification of pHi with a NH4Cl pulse. In the control situation, the pHi recovery rate was 0.118 ± 0.001 (n = 52) pH units/min and ANG II (10−12 M or 10−9 M) increased this value (by 106% or 32%, respectively) but ANG II (10−7 M) decreased it to 47%. The control [Ca2+]i was 99 ± 4 (n = 45) nM and ANG II increased this value in a dose-dependent manner. The ANG II effects on cell volume were minor and late
and should not interfere in the measurements of pHi recovery and [Ca2+]i. To document the signaling pathways in the hormonal effects we used: Staurosporine (a PKC inhibitor), W13 (a calcium-dependent
calmodulin antagonist), H89 (a PKA inhibitor) or Econazole (an inhibitor of cytochrome P450 epoxygenase). Our results indicate
that the biphasic effect of ANG II on Na+/H+ exchanger is a cAMP-independent mechanism and is the result of: 1) stimulation of the exchanger by PKC signaling pathway
activation (at 10−12 – 10−7 M ANG II) and by increases of [Ca2+]i in the lower range (at 10−12 M ANG II) and 2) inhibition of the exchanger at high [Ca2+]i levels (at 10−9 – 10−7 M ANG II) through cytochrome P450 epoxygenase-dependent metabolites of the arachidonic acid signaling pathway. 相似文献
18.
T. V. Roslyakova O. V. Molchan A. V. Vasekina E. M. Lazareva A. I. Sokolik V. M. Yurin A. H. de Boer A. V. Babakov 《Russian Journal of Plant Physiology》2011,58(1):24-35
Two barley cultivars (Hordeum vulgare L., cvs. Elo and Belogorskii) differing in salt tolerance were used to study 22Na+ uptake, expression of three isoforms of the Na+/H+ antiporter HvNHX1-3, and the cellular localization of these isoforms in the elongation zone of seedling roots. During short
(1 h) incubation, seedling roots of both cultivars accumulated approximately equal quantities of 22Na+. However, after 24-h incubation the content of 22Na+ in roots of a salt-tolerant variety Elo was 40% lower than in roots of the susceptible variety Belogorskii. The content of
22Na+ accumulated in shoots of cv. Elo after 24-h incubation was 6.5 times lower than in shoots of cv. Belogorskii and it was 4
times lower after the salt stress treatment. The cytochemical examination revealed that three proteins HvNHX1-3 are co-localized
in the same cells of almost all root tissues; these proteins were present in the tonoplast and prevacuolar vesicles. Western
blot analysis of HvNHX1-3 has shown that the content of isoforms in vacuolar membranes increased in response to salt stress
in seedling roots and shoots of both cultivars, although the increase was more pronounced in the tolerant cultivar. The content
of HvNHX1 in the seedlings increased in parallel with the enhanced expression of HvNHX1, whereas the increase in HvNHX2 and HvNHX3 protein content was accompanied by only slight changes in expression of respective
genes. The results provide evidence that salt tolerance of barley depends on plant ability to restrict Na+ transport from the root to the shoot and relies on regulatory pathways of HvNHX1-3 expression in roots and shoots during
salt stress. 相似文献
19.
The expression of Na+, K+-ATPase α3 subunit and synaptosomal membrane Na+, K+-ATPase activity were analyzed after administration of ouabain and endobain E, respectively commercial and endogenous Na+, K+-ATPase inhibitors. Wistar rats received intracerebroventricularly ouabain or endobain E dissolved in saline solution or Tris–HCl,
respectively or the vehicles (controls). Two days later, animals were decapitated, cerebral cortex and hippocampus removed
and crude and synaptosomal membrane fractions were isolated. Western blot analysis showed that Na+, K+-ATPase α3 subunit expression increased roughly 40% after administration of 10 or 100 nmoles ouabain in cerebral cortex but
remained unaltered in hippocampus. After administration of 10 μl endobain E (1 μl = 28 mg tissue) Na+, K+-ATPase α3 subunit enhanced 130% in cerebral cortex and 103% in hippocampus. The activity of Na+, K+-ATPase in cortical synaptosomal membranes diminished or increased after administration of ouabain or endobain E, respectively.
It is concluded that Na+, K+-ATPase inhibitors modify differentially the expression of Na+, K+-ATPase α3 subunit and enzyme activity, most likely involving compensatory mechanisms. 相似文献
20.
Haibo Xue Weiwei Wang Zhongyan Shan Yuanbin Li Yushu Li Xiaochun Teng Yun Gao Chenling Fan Weiping Teng 《Biological trace element research》2011,143(1):292-301
Iodine is an essential trace element for thyroid hormone synthesis and metabolism, either low or high intake may lead to thyroid
disease, but the pathogenetic mechanisms by which iodine interacts with the thyroid autoimmune are poorly understood. We investigated
the dynamic changes of CD4+CD25+ regulatory T cells in NOD.H-2h4 mice with iodine-induced autoimmune thyroiditis (AIT), and explore potential immune mechanism of AIT induced by iodine. NOD.H-2h4 mice were randomly divided into two groups, and received plain water or water containing 0.005% sodium iodide. Eight weeks
after iodine provision, the incidences of thyroiditis, relative weights of thyroids, and serum thyroglobulin antibody titers
in the iodine-supplied groups were significantly increased compared to the control groups (p < 0.05). The AIT mice had fewer CD4+CD25+Foxp3+ T cells and reduced Foxp3 mRNA expression in splenocytes compared with the controls (p < 0.01), and maintained relatively low levels during the development of thyroiditis. The changes described above aggravated
gradually with the extension of iodine treatment. These data suggest that CD4+CD25+ regulatory T cells may be involved in the pathogenesis and development of AIT induced by iodine. 相似文献