Although aluminum is ubiquitously present on Earth, it is not necessary for life. Aluminum is a metal element that can induce neurotoxicity. The neurotoxicity of aluminum is mainly caused by the aggregation of abnormally phosphorylated tau protein to form neurofibrillary tangles (NFTs). The phosphorylation of tau is regulated by both kinases and phosphatases. ERK is involved in PHF-type tau hyperphosphorylation. Recent studies have revealed that the interaction between microRNAs (miRNAs) and the ERK/MAPK cascade is related to maintaining the normal function of the nervous system. miR-195 is involved in the early development of AD with a potential impact on cognition. Therefore, we speculate that miRNA-195 may regulate ERK activity, thereby causing hyperphosphorylation of tau protein and neurotoxicity. The purpose of this study was to explore the role of miRNA-195-5p in regulating ERK in the process of aluminum maltol-induced tau hyperphosphorylation. The results showed that aluminum exposure decreased the expression level of miRNA-195-5p and increased the expression of P-ERK, abnormal phosphorylated tau. After inhibiting the activity of ERK, the expression of phosphorylation tau protein decreased. There is an interaction effect between inhibiting the activity of ERK and aluminum exposure on the expression of phosphorylated tau proteins. After the overexpression of miRNA-195-5p, the activity of ERK was inhibited. There is an interaction effect between miRNA-195-5p and aluminum exposure on the expression of phosphorylated tau. In conclusion, miRNA-195-5p regulates ERK involvement in the abnormal phosphorylation of tau protein by Al (mal)3in PC12 cells.

Objectives: To evaluate the risk of cognitive impairment in workers with plasma aluminum concentrations and lifestyles using a Bayesian network (BN). Methods: In 2019, 476 male workers in the Shanxi Aluminum factory were investigated. We measured plasma aluminum concentrations in workers by inductive coupled plasma mass spectrometry (ICP-MS) and tested workers' cognitive function by the MoCA scale. We collected the data of lifestyle by the occupational Workers' Health questionnaire and express the influence of lifestyle on cognition by the OR value (95 %CI) of logistic regression. A Bayesian network model was used to predict the risk of cognitive dysfunction. Results: The subjects were divided into a cognitively normal group and cognitively impaired group according to MoCA scores. There were statistically significant differences in age, education level, alcohol consumption, physical exercise, reading, aluminum length of service and blood aluminum concentration between the two groups (P < 0.05). The plasma aluminum concentration in the cognitive impairment group was 1.68 times higher than that in the cognitive normal group. Four groups were established according to the quartile of blood aluminum concentration of the subjects, namely, Group Q1 (<14.95 mu g/L), Q2 group (14.95-32.96 mu g/L), Q3 group (32.96-56.62 mu g/L), and Q4 group (>56.62 mu g/L). Binary logistic regression analysis showed that in the adjustment variable Model2, drinking, short sleep, long sleep, and mobile phone use increased the risk of cognitive impairment by 1.505(0.99,2.289), 1.269(0.702,2.295), 1.125(0.711,1.781) and 1.19(0.779,1.82), respectively, compared with their reference values. The risk of cognitive impairment from reading and exercise was 0.7(0.398,1.232) and 0.787(0.51,1.217), respectively, compared with those of no reading and no exercise. The risk of cognitive impairment of blood aluminum concentration in the Q2, Q3, and Q4 groups was 2.103 (1.092,4.051), 1.866(0.955,3.644) and 3.679(1.928,7.020), respectively, compared with that in the Q1 group. Compared with age <40 , the risk of cognitive impairment of age >= 40 was 2.515(1.508,4.193) (P < 0.05). Bayesian network model results showed that if all participants had plasma aluminum concentrations higher than Q4, the prevalence of cognitive impairment was 54.5 %. The prevalence of cognitive impairment was 75.0 % if all participants had plasma aluminum levels above Q4, were older than 40, smoked, drank alcohol, used a cell phone for more than 2 h, slept for more than 8 h, did not exercise, and did not read. Conclusions: Our findings suggest that both poor lifestyle and occupational aluminum exposure may affect cognitive function. Workers must maintain a reasonable lifestyle and reduce aluminum exposure, which can control the occurrence of cognitive impairment.

BackgroundOccupational aluminum exposure may associate with cognitive impairment in workers. At present, brain functional imaging data are not available for evaluating cognitive dysfunction in workers with occupational exposure to aluminum. The role of brain functional connectivity in cognitive decline associated with occupational aluminum exposure is not clear yet. ObjectiveTo explore potential mediating effect of brain functional connectivity value on cognitive decline induced by occupational aluminum exposure, to assess the relationship between cognitive impairment and brain functional connectivity, and to identify appropriate imaging evidence of early cognitive changes induced by occupational aluminum exposure. MethodsThis study used a subset data from a previous cross-sectional survey. Based on the data of aluminum-exposed workers, over 40 years old, aluminum-exposed working years >1 year, Montreal International Cognitive Assessment (MoCA) (Beijing version) score <26 points, 20 workers were selected as the case group, and 40 healthy workers with the same basic conditions (age, smoking, drinking, etc.) in non-aluminum production were selected as the control group with a 1∶2 matching ratio. The basic information of the subjects was collected, plasma aluminum level and cognitive function level were evaluated, and different brain functional connectivity values of default mode network (DMN) were measured by magnetic resonance imaging. The mediating effect analysis was conducted to examine the role of brain functional connectivity in the relationship between aluminum exposure and cognitive function. ResultsThe plasma aluminum concentration of the case group was 1.76 times higher than that of the control group [(33.04±12.02) µg·L−1 vs (18.74±8.95) µg·L−1, P<0.05]; the MoCA score was 9.5 points lower [(18.35±2.64) vs (27.85±0.92), P<0.05]. The mean functional connection values of DMN1 and DMN2 in the case group were lower than those in the control group (P<0.05). The mean functional connection values of the left precuneus, left middle cingulate cortex, left superior medial gyrus, left precentral gyrus, and left cerebellum also decreased in the case group compared with the control group (P<0.05). Plasma aluminum concentration was negatively correlated with DMN1 functional connectivity value and MoCA scores (b=−0.004, 95%CI: −0.008–−0.001; b=−0.15, 95%CI: −0.233–−0.067; P<0.05). The mean functional connection values of DMN1 and DMN2 were positively correlated with MoCA scores (b=10.945, 95%CI: 5.574–16.316; b=10.107, 95%CI: 2.457–17.758; P<0.05). With the increase of plasma aluminum concentration, MoCA score decreased, but when the plasma aluminum concentration exceeded 19.50 µg·L−1, MoCA score decreased slowly. With the increase of the mean functional connectivity value of DMN1, MoCA score increased, but when the mean functional connectivity value of DMN1 exceeded 1.05 and continued to increase, the increase of MoCA score slowed down. The results of mediating effect analysis showed that the functional connectivity value of DMN1 partially mediated the relationship between plasma aluminum concentration and MoCA score, and the mediating effect was 25.80%. ConclusionCognitive impairment in occupational aluminum-exposed workers is closely related to brain resting-state functional connectivity. There is a dose-response relationship of plasma aluminum concentration with DMN1 functional connectivity value and MoCA scores, and DMN1 functional connectivity value partially mediates the relationship between plasma aluminum concentration and MoCA scores. The brain functional connectivity value can be used as meaningful imaging data to study the cognitive decline induced by chronic aluminum exposure.

BackgroundAluminum activates signal transducer and activator of transcription 3 (STAT3), causing microglial nucleotide-binding and oligomerization domain-like receptors protein 3 (NLRP3) inflammasome activation and inflammatory responses and producing neurotoxicity.ObjectiveTo explore the role of STAT3 regulated NLRP3 inflammasomes in the inflammatory response of mouse microglia cell line (BV2) cells induced by maltol aluminum [Al(mal)3].MethodsBV2 cells were assigned to five groups: one control group, three Al(mal)3 exposure groups (low, medium, and high doses at 40, 80, and 160 μmol·L−1 Al(mal)3 respectively), and one C188-9 (STAT3 antagonist) intervention group [10 μmol·L−1 C188-9 +160 μmol·L−1 Al(mal)3]. Cell viability was detected by CCK8. The expression of M1/M2 type markers, i.e. CD68/CD206, STAT3, p-STAT3, NLRP3, cleaved-casepase-1, and apoptosis-associated speck-like protein (ASC) in BV2 cells were detected by Western blotting, and proinflammatory cytokines interleukin (IL)-1β and IL-18, and anti-inflammatory cytokine IL-10 were determined by ELISA.ResultsThe results of cell viability assay showed that cell viability gradually decreased with the increase of Al(mal)3 dose. Compared with the control group, the cell viability of the Al(mal)3 high-dose group was decreased by 18% (P<0.05); compared with the Al(mal)3 high-dose group, the cell viability of the C188-9 intervention group was significantly elevated by 14% (P<0.05). Compared with the control group, the expression levels of CD68 in the Al(mal)3 low-, medium-, and high-dose groups were elevated by 19%, 20%, and 21%, respectively (P<0.05); the expression level of CD206 in the Al(mal)3 high-dose group was decreased by 25% (P<0.05). Compared with the Al(mal)3 high-dose group, the expression level of CD68 in the C188-9 intervention group was reduced by 9% (P<0.05), whereas the expression level of CD206 was elevated by 22% (P<0.05). Compared with the control group, the p-STAT3 protein expression and the p-STAT3/STAT3 ratio in the Al(mal)3 high-dose group increased by 129% and 127%, respectively (P<0.05). Compared with the Al(mal)3 high-dose group, the p-STAT3 protein expression and the p-STAT3/STAT3 ratio in the C188-9 intervention group were decreased by 55% and 54%, respectively (P>0.05). Compared with the control group, the expression level of NLRP3 protein increased by 75% in the Al(mal)3 high-dose group (P<0.05), the expression levels of cleaved-casepase-1 protein increased by 28% and 35% in the Al(mal)3 medium- and high-dose groups (P<0.05), and the expression levels of ASC increased by 22%, 25%, and 53% in the Al(mal)3 low-, medium- and high-dose groups (P<0.05), respectively. Compared with the Al(mal)3 high-dose group, the expression levels of NLRP3, cleaved-casepase-1, and ASC proteins in the C188-9 intervention group decreased by 30%, 19%, and 32%, respectively (P<0.05). Compared with the control group, the levels of IL-1β in the Al(mal)3 medium- and high-dose groups increased by 18% and 21%, respectively (P<0.05), and the level of IL-18 in the Al(mal)3 high-dose group increased by 10% (P<0.05). Compared with the Al(mal)3 high-dose group, the IL-18 levels were reduced by 23% in the C188-9 intervention group (P<0.05). The content of anti-inflammatory factor IL-10 did not differ significantly between groups (P>0.05).ConclusionAluminum can induce inflammatory responses in BV2 microglia and is predominantly pro-inflammatory, and the mechanism may involve STAT3 regulation of NLRP3 inflammasome secretion of inflammatory factors.

This study investigates the effects of lithium and caffeine on psychomotor activities, defecation, and gastric lesions induced by restraint stress. Rats exposed to restraint stress typically exhibited a biphasic response consisting of an initial hypermotility (such as tail-flipping, body-rolling, jaw movement, and vocalization) accompanied by defecation, and followed by hypomotility (decrease in motility) accompanied by gastric ulceration. Lithium chloride (150 micrograms, ICV; 50 and 100 mg/kg, IP) significantly attenuated these responses while N6-cyclohexyl adenosine (CHA; 1.5 micrograms, ICV; 0.3 mg/kg, IP), a potent adenosine A1 receptor agonist, attenuated the behavioral effects but potentiated the gastric ulceration. Caffeine (3 micrograms, ICV; 1.0 mg/kg, IP), an adenosine receptor antagonist, inhibited the effects of CHA in animals exposed to 3 h of stress, but aggravated the effects in animals exposed to 6-12 h of stress. These results suggest that caffeine consumption may produce supersensitivity of adenosine receptors, which potentiate the actions of adenosine or CHA. Lithium may modulate the effects of stress by indirectly inhibiting central adenosine receptor activity.

BackgroundOccupational aluminum exposure is closely related to cognitive impairment, and alcohol consumption is also closely related to cognitive dysfunction.ObjectiveTo explore the effects of types of alcohol consumption on cognitive function of occupational aluminum exposed workers.MethodsA total of 181 workers aged from 23 to 56 years were selected by cluster sampling method in an electrolytic aluminum workshop of an aluminum plant in a region and in a maintenance workshop of another plant in the same region from July to August, 2019. Venous blood was collected, and plasma aluminum concentration was determined by inductively coupled plasma mass spectrometry. The study subjects were divided into low and high exposure groups based on the median blood aluminum level and type of work. Their basic information was collected by occupational health examination. Workers' cognitive function was assessed using the Montreal Cognitive Assessment Scale-Beijing Edition. Logistic regression was used to analyze the association between plasma aluminum concentration and cognitive impairment, and between the types of alcohol consumption (including Baijiu, red wine, and beer) and cognitive impairment, Unconditional logistic regression was used to fit multiplicative interaction model as well as additive interaction model of plasma aluminum concentration and the types of alcohol consumption, and to calculate the relative excess relative risk due to interaction (RERI) and attributable proportion due to interaction (AP).ResultsThe M (P25, P75) concentrations of plasma aluminum were 40.01 (25.05, 60.56) µg·L−1 in the total study subjects, 25.16 (17.13, 34.78) µg·L−1 in the low exposure group and 60.56 (47.40, 68.53) µg·L−1 in the high exposure group. After adjusting the type of alcohol consumption, drinking, age, duration of exposure to aluminum, education, marital status, and smoking, the odds ratios for impairments of attention, language expression, and overall cognitive function in the high exposure group were 4.295 (95%CI: 1.912-9.648), 5.687 (95%CI: 1.355-23.867), and 2.720 (95%CI: 1.225-6.040) times of the low exposure group respectively. Besides, after adjusting blood aluminum concentration, total alcohol consumption, age, duration of exposure to aluminum, education, marital status, and smoking, the risk of attention impairment of the Baijiu drinkers was 2.613 (95%CI: 1.054 to 6.837) times of the non-Baijiu drinkers; the risks of impairment of visuospatial abilities and execution functions, language expression, delayed recall, and overall cognitive function of the beer drinkers were 3.165 (95%CI: 1.285-7.797), 17.898 (95%CI: 1.590-201.480), 3.118 (95%CI: 1.215-8.003), and 3.824 (95%CI: 1.736-8.423) times of the non-beer drinkers. There were both additive [RERI (95%CI): 1.745 (1.394-2.097), AP (95%CI): 0.415 (0.201-0.630)] and multiplicative (OR=3.591, 95%CI: 1.393-9.255) interactions between Baijiu intake and plasma aluminum concentration levels on the attention domain. The cognitive impairment attributed to the interactive effects of drinking Baijiu and plasma aluminum concentration in individuals with attention impairment accounted for 41.5%. There were both additive [RERI (95%CI): 5.955 (0.562-11.328), AP (95%CI): 0.829 (0.577-1.081)] and multiplicative (OR=42.174, 95%CI: 5.469-325.252) interactions between beer drinking and plasma aluminum concentration on the overall cognitive function. Among the individuals with overall cognitive impairment, the cognitive impairment caused by the interaction of beer drinking and plasma aluminum concentration accounted for 82.9%.ConclusionOccupation aluminum exposed workers' attention, language expression, and overall cognitive function are closely related to their plasma aluminum concentration. Plasma aluminum concentrations have interactions with Baijiu and beer consumption on cognitive impairment of workers.

Background: Aluminum (Al) is recognized as a neurotoxin. Studies have confirmed that the neurotoxicity induced by Al may be related to tau hyperphosphorylation. Phosphorylated tau is degraded through the ubiquitin-proteasome pathway (UPP), in which the carboxyl terminus of Hsc70-interacting protein (CHIP) plays an important role. However, whether the CHIP-mediated UPP plays a role in regulating tau hyperphosphorylation induced by Al is not yet known. Objective: To explore the molecular mechanism of the CHIP-mediated UPP in tau hyperphosphorylation induced by AlCl3 in N2a cells. Methods: Mouse neuroblastoma cells (N2a) were exposed to different concentrations of AlCl3 (0, 0.5, 1, and 2 mM) and treated with CHIP/CHIP (ΔU-box)/CHIP (ΔTPR) plasmid transfection. The cell viability was determined by CCK-8 kit. Protein expression was detected by Western blot. The interaction between CHIP and AlCl3 exposure on the proteins was analyzed by factorial design ANOVA. Results: With the increase of AlCl3 exposure, N2a cell viability decreased (P<0.05), and the expressions of tau-5, pThr231, pSer262, pSer396, CHIP, Hsp70 and Ub proteins increased (P<0.05). Compared with 1 mM AlCl3 group, the expressions of pThr231, pSer262, and pSer396 were significantly decreased (P<0.05) after CHIP overexpression; the expressions of pThr231, pSer262, and pSer396 were significantly increased (P<0.05) after CHIP (ΔU-box) transfection or CHIP (ΔTPR) transfection. Factorial analysis showed that there were interactions between CHIP overexpression and AlCl3 exposure in the protein expressions of CHIP, Ub, pThr231, pSer262, and pSer396 (P<0.05). Conclusions: Al can cause tau hyperphosphorylation, mainly affecting the pThr231, pSer262, and pSer396 sites of tau in N2a cells. UPP is involved in the degradation of tau hyperphosphorylation induced by Al in N2a cells, of which CHIP may be the main regulatory target. Both the U-box and TPR domains of CHIP are indispensable and play an important role in the regulation of tau hyperphosphorylation induced by AlCl3 in N2a cells.

Objective To evaluate the risk factors of occupational aluminum exposure on workers’ executive function.Methods A total of 172 aluminum-exposed workers were selected by convenient sampling method. According to the blood aluminum concentration, the subjects were divided into low-, medium-, and high-level groups. The trail making test（TMT） was used to evaluate the executive function and its risk factors of the subjects. Results The median and 25th and 75th percentiles [M(P 25 , P 75 )] of blood aluminum was 23.71（13.14, 38.27） μg/L. The M(P 25 , P 75 ) of blood aluminum levels in low-, medium-and high-level groups were 9.84（2.60, 13.18）, 23.18（19.45, 28.23） and 45.02（38.23, 62.52） μg/L, respectively.The total time and abnormality rate of TMT-A, TMT-B and TMT in this study increased with the increasing blood aluminum levels（all P＜0.05）. The results of binary logistic regression analysis showed that the abnormal risks of total time on TMT-B and TMT in the medium-level group were 2.59 and 2.98 times respectively（both P＜0.05）, and the abnormal risks of total time on TMT-A, TMT-B and TMT in the high-level group were 7.77, 11.04 and 9.74 times respectively compared with the low-level group（all P＜0.05）. The longer the length of service, the higher the abnormal risk of total time on TMT-B and TMT（both P＜0.05）. The higher the education level, the lower the risk of abnormal risk of total time on TMT-A and TMT（both P＜0.05）.Conclusion Occupational aluminum exposure may impair the executive function of workers with a dose-effect relationship.Blood aluminum level and length of employment are risk factors and education level is a protective factor for the executive function of workers.

Objective: To explore the effects of occupational aluminium(Al) exposure on workers' cognition through a longitudinal study. Methods: The study population consisted of 276 workers in an Al factory. In 2014, we used inductively coupled plasma mass spectrometry (ICP-MS) to determine the plasma aluminium (P-Al) concentration of the workers, and a combined questionnaire to test the workers' cognitive function. Followed-up in 2016, the workers were tested again for cognitive function. Generalized linear regression was used to assess the association between P-Al concentration and cognitive scores, and multivariable logistic regression was used to assess the risk of cognitive decline caused by Al exposure. Results: Generalized linear regression results showed that a non-significant association was found between the P-Al concentration and cognitive test scores (P > 0.05) in 2014. Two years later, each 10-fold increase in P-Al concentration was inversely associated with the score of Mini-Mental state examination (MMSE) (beta: -0.53, 95% CI: -0.86, -0.20) and Fuld object memory evaluation (FOME) (beta: -0.93, 95% CI: -1.62, -0.24). Each 10-fold increase in P-Al concentration was inversely associated with MMSE2016-2014 (beta: -0.38, 95% CI: -0.74, -0.01) and FOME2016-2014 (beta: -1.20, 95% CI: -1.95, -0.45). There was a statistically significant difference in the average annual rate of change of MMSE and FOME with the tertile of P-Al concentration increase (P < 0.05). The multivariable logistic regression results showed that as the P-Al concentration increased, the risk of a FOME score decline increased (P-trend = 0.009). Conclusions: Continuous occupational Al exposure can damage workers' overall cognitive ability, especially episodic memory function. (C) 2021 Elsevier Ltd. All rights reserved.

To evaluate the different characteristics of cognitive impairment caused by occupational aluminium exposure at different ages, we surveyed 1660 workers in Shanxi Aluminium Plant, China, and assessed their cognitive function and plasma aluminium concentration. In multiple linear regression, the scores of the digit-span test (DST) and digit-span backward test (DSBT) were negatively correlated with plasma aluminium concentration when concentration reached 34.52 ?g/L in younger group (<40 years), while in the middle-aged group (?40 years) only found when concentration reached 42.25 ?g/L (?<0, P < 0.05). In logistic regression, when plasma aluminum concentration reached 42.25?g/L, odds ratios (95 % confidence interval) were 1.695 (1.062?2.705) and 3.270 (1.615?6.620) for DST, 7.644 (3.846?15.192) and 15.308 (4.180?56.059) for DSBT in middle-aged group and younger group, respectively. These results showed that aluminium exposures were associated with cognitive impairment among aluminium-exposed workers, particularly for young workers who were more susceptible.

Aluminum (Al) is an environmental neurotoxin to which humans are extensively exposed; however, the molecular mechanism of aluminum toxicity is unclear. Several studies have indicated that exposure to aluminum can cause abnormal phosphorylation of the tau protein. The purpose of this study was to investigate respectively the special molecular mechanism of abnormal regulation on synthesis and degradation of the tau protein induced by AlCl3 in cells of different species. The results of tau protein showed that the sites of abnormal tau phosphorylation induced by AlCl3 are Thr231, Ser262, and Ser396 in N2a cells. Meanwhile, the expressions of Thr181, Thr231, and Ser262 increased abnormally in SH-SY5Y cells. The result of the study showed that PP2A expression was high in N2a cells, while GSK-3β and PP2A in SH-SY5Y cells were involved in the synthesis process of abnormal tau phosphorylation induced by AlCl3. In N2a cells, the ubiquitin-proteasome pathway (UPP) mainly regulated tau phosphorylation at Ser262 and Ser396. Meanwhile, in SH-SY5Y cells, the UPP mainly regulated tau phosphorylation at Thr231 and Ser396. In summary, the UPP is involved in the degradation of Tau that is abnormally phosphorylated induced by AlCl3, but this process is site-specific and differs in cells of different species.

目的 探讨职业性铝接触对男性工人血液系统的影响.方法 采用整群抽样法,选择某铝厂电解车间249名男性铝作业工人为研究对象.采集其血样测定血铝水平与血常规;根据血铝水平三分位数(P33为13.9μg/L,P67为37.7 μg/L)将研究对象分为低、中、高水平组.结果 高水平组人群红细胞计数和血红蛋白水平均低于低水平组(P＜0.05);中水平组人群红细胞计数和血红蛋白水平分别与低、高水平组比较,差异均无统计学意义(P＞0.05).3组人群白细胞计数与血小板计数比较,差异均无统计学意义(P＞0.05).广义线性回归模型分析结果显示,控制年龄、工龄、文化程度、吸烟、饮酒等混杂因素后,血铝水平越高,铝作业工人红细胞计数与血红蛋白水平均越低(P＜0.05).结论 职业性铝接触可导致工人红细胞计数和血红蛋白水平下降,呈剂量-效应关系.

Objective To explore the role of OPN in the pathogenesis of immune thrombocytopenia (ITP) by detecting the content of plasma osteoponetontin (OPN) in patients with primary ITP before and after treatment and in normal controls. Methods Peripheral venous blood (5 ml) was collected from 40 healthy adults (control group) and 40 ITP patients before and after treatment. The collected samples were centrifuged to separate the plasma. Enzyme-linked immunosorbent assay (ELISA) was used to measure the content of OPN in the samples to observe the expression of OPN in the control group, the pre-treatment group, and the post-treatment group. The correlation was analyzed between platelet count and plasma OPN expression in ITP patients, and OPN contents were compared between the effective group and the ineffective group before and after treatment. Results Plasma OPN level in the pre-treatment group was significantly higher than that in the control group (P<0.05). Plasma OPN level in the post-treatment group showed a significantly decreasing trend compared with that the pre-treatment group (P<0.05). There was a significant negative correlation between platelet count and plasma OPN expression in ITP patients (r=-0.80, P<0.05). After treatment, the effective rate was 92.5% (37/40) and the ineffective rate was 7.5% (3/40). The OPN change between before and after treatment was significantly higher in the effective group than in the ineffective group (P<0.05). Conclusion OPN may be involved in the pathogenesis of ITP, which is correlated with the degree of thrombocytopenia. Monitoring the change of OPN content between before and after treatment may provide a reference for evaluating the therapeutic efficacy for ITP. Key words: Primary immune thrombocytopenia; Osteopontin; Autoimmunity