Does medical insurance improve health? An empirical analysis from China.

BACKGROUND: Medical insurance is considered to be closely related to individual health status, while their relationship are left to be clarified. This article aims to examine the relationship between medical insurance and the health status of residents in China. METHODS: The data is from a nationally representative sample of CGSS2015, and the estimation methods of ordered logit model, generalised ordered logit model and instrumental variable (IV) were used. RESULTS: Both public medical insurance (PMI) and commercial medical insurance (CMI) had a positive correlation with residents' self-assessed physical and mental health, while PMI was more statistically significant and substantively important than CMI. The basic results estimated with the generalised ordered logit model and IV model still remained robust. Further analysis found that medical insurance, whether public or commercial, had more or less weakened the importance of income to personal health, showing a substitute effect for income. CONCLUSION: PMI has been proven to help promote the physical and mental health of residents and moderate the importance of residents' income to health. Besides, CMI also plays a beneficial supplementary role in promoting residents' health.

Protective effect of omega-3 polyunsaturated fatty acids on sepsis via the AMPK/mTOR pathway.

CONTEXT: Sepsis is a systemic inflammatory response caused by infection, with high morbidity and mortality. Omega-3 polyunsaturated fatty acids (ω-3 PUFAs) have reported biological activities. OBJECTIVE: This study explored the signaling pathways through which ω-3 PUFAs protect against sepsis-induced multiorgan failure. MATERIALS AND METHODS: Septic Sprague-Dawley (SD) rat model was established by the cecum ligation perforation (CLP) method. Rats were divided into control, sham, model, parenteral ω-3 PUFAs (0.5 g/kg) treatment, ω-3 PUFAs (0.5 g/kg) + AMPK inhibitor Compound C (30 mg/kg) treatment, and ω-3 PUFAs (0.5 g/kg) + mTOR activator MHY1485 (10 mg/kg) treatment groups. The serum inflammatory cytokines were measured using ELISA. Organ damage-related markers cTnI, CK, CK-MB, Cr, BUN, ALT, and AST were measured using an automated chemical analyzer. The AMPK/mTOR pathway in liver, kidney, and myocardial tissues was detected using western blot and qRT-PCR methods. RESULTS: CLP treatment enhanced the secretion of pro-inflammatory cytokines and multi-organ related markers, along with increased p-AMPK/AMPK ratio (from 0.47 to 0.87) and decreased p-mTOR/mTOR ratio (from 0.33 to 0.12) in rats. The inflammation response and multi-organ injury induced by CLP treatment could be partially counteracted by 0.5 g/kg parenteral ω-3 PUFA treatment. The activated AMPK/mTOR pathway in CLP-induced rats was further promoted. Finally, Compound C and MHY1485 could reverse the effects of parenteral ω-3 PUFA treatment on sepsis rats. DISCUSSION AND CONCLUSION: ω-3 PUFAs ameliorated sepsis development by activating the AMPK/mTOR pathway, serving as a potent therapeutic agent for sepsis. Further in vivo studies may validate potential clinical use.

A Novel Inhibitor of Homodimerization Targeting MyD88 Ameliorates Renal Interstitial Fibrosis by Counteracting TGF-ß1-Induced EMT in Vivo and in Vitro.

BACKGROUND/AIMS: The TLR/MyD88/NF-κB signaling pathway has been successfully used to treat renal interstitial fibrosis (RIF). However, the exact therapeutic mechanism is still unknown. Here, we assessed the therapeutic efficacy of TJ-M2010-2, a small molecular compound that inhibits MyD88 homodimerization, in RIF induced by ischemia reperfusion injury (IRI). METHODS: In vivo, RIF was induced in mice by IRI, and the mice were prophylactically treated with TJ-M2010-2. In vitro, HK-2 cells were incubated with TGF-ß1 to induce EMT, and the cells were pretreated with TJ-M2010-2. RESULTS: We found that, compared with the IRI group, the TJ-M2010-2 group showed marked attenuation of RIF and renal function injury; decreased expression of TGF-ß1, α-SMA, vimentin, MMP2 and MMP9; and increased E-cadherin expression. Furthermore, TGF-ß1-induced EMT was blocked by TJ-M2010-2 in HK-2 cells, as evidenced by blocked morphologic transformation, restored E-cadherin expression and inhibited α-SMA expression. In addition, compared to the TGF-ß1 group, the TJ-M2010-2 group showed profound inhibition of the expression of TRAF6, p65 and Snail and upregulation of the expression of IκBα. CONCLUSION: This MyD88 inhibitor may be a potential therapeutic agent to ameliorate RIF.

Astrocyte elevated gene-1 promotes invasion and epithelial-mesenchymal transition in bladder cancer cells through activation of signal transducer and activator of transcription 3.

OBJECTIVES: To determine the impact of astrocyte elevated gene-1 on the invasion and epithelial-mesenchymal transition of bladder cancer cells in vitro and metastasis in vivo. METHODS: Gain- and loss-of-function studies were carried out to investigate the biological roles of astrocyte elevated gene-1 in bladder cancer cell invasion, epithelial-mesenchymal transition and lung metastasis. The mechanism underlying the activity of astrocyte elevated gene-1 was examined. RESULTS: Overexpression of astrocyte elevated gene-1 led to a significant increase in the invasive ability of UMUC3 and T24 bladder cancer cells in Matrigel invasion assays. In contrast, silencing of astrocyte elevated gene-1 restrained bladder cancer cell invasion. Overexpression of astrocyte elevated gene-1 downregulated E-cadherin and upregulated vimentin and Twist1, while silencing of astrocyte elevated gene-1 exerted an opposite effect. Mechanistically, astrocyte elevated gene-1 overexpression promoted the phosphorylation of signal transducer and activator of transcription 3 in bladder cancer cells. Treatment with WP1066, a specific signal transducer and activator of transcription 3 inhibitor, significantly abolished astrocyte elevated gene-1-induced invasion and epithelial-mesenchymal transition in UMUC3 cells. In vivo studies showed that astrocyte elevated gene-1 overexpression stimulated the growth of UMUC3 xenograft tumors and lung metastasis. CONCLUSIONS: Astrocyte elevated gene-1 shows the ability to promote bladder cancer metastasis, which is causally linked to induction of signal transducer and activator of transcription 3 activation and epithelial-mesenchymal transition. Therefore, targeting astrocyte elevated gene-1 might offer therapeutic benefits in treating metastatic bladder cancer.

The Relationship between Neighborhood Social Capital and the Health of Chinese Urban Elderly: An Analysis Based on CHARLS2018 Data.

There is growing interest in the relationship between neighborhood social capital and the health of urban older people, but existing research still falls short in exploring the relationship between the two. Based on 2018 CHARLS data, this paper quantitatively examines the association between neighborhood social capital and the self-rated health of urban older people. The study found that, after controlling for a series of variables, both increased social interaction and increased frequency of social interaction significantly improved urban older people's self-rated health. To implement the Health China strategy and improve the health of urban older people, further attention should be paid to the role of neighborhood social capital, creating a harmonious environment for neighborhood interaction and promoting the cultivation of neighborhood social capital.

WD repeat protein 54-mediator of ErbB2-driven cell motility 1 axis promotes bladder cancer tumorigenesis and metastasis and impairs chemosensitivity.

One of the most abundant protein-protein interaction domains in the human proteome is the WD40 repeat (WDR) domain. A Gene Expression Omnibus dataset revealed 37 differentially expressed WDR domain genes in bladder cancer (BC). WD repeat domain 54 (WDR54), an upregulated WDR domain gene, was selected for further investigation. Sixty pairs of frozen BC tumor and non-malignant bladder tissues and 83 paraffin-embedded BC tissue specimens were obtained. Loss-/gain-of-function experiments were carried out using BC and xenograft tumor models. WDR54 was overexpressed in BC cells, and its high expression was linked to tumor stage and lymph node metastases in patients. WDR54 contributed to the tumorigenesis and metastasis of BC and impaired its chemosensitivity. WDR54 prevented the degradation and ubiquitination of the mediator of ErbB2-driven cell motility 1 (MEMO1). WDR54 also promoted the interaction between MEMO1 and insulin receptor substrate 1 (IRS1) and activated the IRS1/AKT/ß-catenin pathway in BC cells. Particularly, WDR54 depended on MEMO1 to exert its biological functions. Our study demonstrated the relevance of WDR54 in BC and provides insight into the molecular mechanism underlying BC.

Experimental study on inhibitory effects of diallyl sulfide on growth and invasion of human osteosarcoma MG-63 cells.

The inhibitory effects of diallyl sulfide (DAS) derived from allicin on in vitro and in vivo proliferation of human osteosarcoma MG-63 cells and the action mechanism, and the influence of DAS on invasive capability of MG-63 cells were investigated in order to search for the novel medicines for osteosarcoma. In the in vitro experiment, MG-63 cells were treated with different concentrations of DSA, and the morphological changes of MG-63 cells were observed under an inverted phase microscope. MTT method was used to assay the proliferation of MG-63 cells. Semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) was used to detect the VEGF mRNA expression level in MG-63 cells. By using Transwell invasion assay, the influence of DAS on invasive ability of MG-63 cells was tested. In the in vivo experiment, the nude mice MG-63 cells tumor-bearing model was established, and different concentrations of DAS were injected beside the tumor. Twenty-one days after treatment, the mice were killed, the tumor size and tumor inhibition rate were calculated. The microvessel density (MVD) was determined by using immunohistochemistry. In the in vitro experiment, different concentrations of DAS could obviously inhibit proliferation of MG-63 cells in a time- and concentration-dependent manner. RT-PCR revealed that the expression levels of VEGF mRNA in DSA groups (different concentrations) were significant reduced as compared with those in control group (all P<0.05). Transwell invasion assay indicated that in 20 and 40 µg/mL DAS groups, the number of migratory cells was 91.4±8.3 and 81.8±7.4 respectively, which was significantly declined as compared with that in control group (150.4±14.7, both P<0.05). In the in vivo experiment, DAS could significantly suppress the growth of MG-63 tumor-bearing tissue. Immunohistochemistry demonstrated that different concentrations (20 and 40 µg/mL) of DAS could significantly decrease MVD of MG-63 tumor-bearing tissue (all P<0.05). It was suggested that DAS could inhibit the growth of MG-63 cells probably by suppressing the expression of VEGF mRNA.

EDARADD silencing suppresses the proliferation and migration of bladder cancer cells.

PURPOSE: Bladder cancer is a kind of common malignant cancer in the urinary system. The expression of EDARADD (ectodysplasin-A receptor-associated death domain) in bladder cancer is higher than the normal samples. However, its role in bladder cancer remains unknown. In the present study, we analyzed the expression of EDARADD in 81 bladder cancer samples by immunohistochemistry as well as its correlation with clinical characteristics. In addition, the role of EDARADD was also explored through loss of function. MATERIALS AND METHODS: Cell proliferation assay and MTT assay were conducted to assess the proliferation of bladder cancer cells and transwell assay and wound healing assay were conducted to assess the migration of bladder cancer cells. On the other hand, the levels of epithelial-mesenchymal transition (EMT) associated proteins and the key molecules in the MAPK signaling pathway were detected by western blot. In vivo experiments were also conducted to determine the effect of EDARADD silencing on the metastasis of bladder cancer cells and the MAPK signaling pathway. RESULTS: EDARADD was highly expressed in bladder cancer samples, especially in high-grade bladder cancer samples. The high EDARADD level indicated a poor survival. Interestingly, EDARADD silencing suppressed the proliferation, migration and EMT of bladder cancer cells. Furthermore, the MAPK signaling pathway was repressed by EDARADD silencing. Additionally, silencing EDARADD also inhibited the metastasis of bladder cancer and the MAPK signaling pathway in vivo. It is indicated that silencing EDARADD may suppress the proliferation and metastasis of bladder cancer cells through the MAPK signaling pathway. CONCLUSION: These results indicate that EDARADD may become a probable target for the treatment of bladder cancer.

Long Noncoding RNA HAND2-AS1 Suppresses Cell Proliferation, Migration, and Invasion of Bladder Cancer via miR-17-5p/KLF9 Axis.

Bladder cancer (BC) is the most common type of malignant tumor in the genitourinary system. Through the microarray analysis of clinical samples, long noncoding RNA HAND2-AS1 expression was found to be downregulated in BC tissues. However, the function of HAND2-AS1 on BC and underlying mechanism are unclear. In this study, the correlations of HAND2-AS1 with clinicopathological parameters in BC patients were determined. The gain- and loss-of-function experiments were conducted to examine the role of HAND2-AS1 in malignant behaviors of BC cells in vitro and in vivo. Then, we paid attention to miR-17-5p/KLF9 axis to illustrate the molecular mechanism. Results showed that HAND2-AS1 was downregulated in BC tissues, and its overexpression significantly inhibited cell proliferation, migration, and invasion in vitro, as well as tumor growth in vivo. Knockdown of HAND2-AS1 caused an opposite effect on BC cell malignancies. Furthermore, miR-17-5p was shown to be a direct target of HAND2-AS1, and it reversed the inhibitory effect of HAND2-AS1 on BC malignancies. Also, as a downstream factor of miR-17-5p, KLF9 silencing was demonstrated to mediate the role of miR-17-5p inhibitor in BC cell proliferation and invasion. Thus, it suggests that HAND2-AS1 acts as a suppressor in BC development through miR-17-5p/KLF9 axis.

Effect of ω-3 polyunsaturated fatty acid on toll-like receptors in patients with severe multiple trauma.

This study examined the effects of ω-3 polyunsaturated fatty acid (ω-3PUFA) on the expression of toll-like receptor 2 (TLR2), toll-like receptor 4 (TLR4) and some related inflammatory factors in peripheral blood mononuclear cells (PBMCs) of patients with early-stage severe multiple trauma. Thirty-two patients who were admitted to the Department of Traumatic Surgery, Tongji Hospital (Wuhan, China) between May 2010 and November 2010, and diagnosed as having severe multiple trauma with a injury severity score (ISS) no less than 16, were enrolled in the study and divided into two groups at random (n=16 in each): ω-3PUFA group and control group in which routine parenteral nutrition supplemented with ω-3PUFA or not was administered to the patients in two groups for consecutive 7 days. Peripheral blood from these patients was collected within 2 h of admission (day 0), and 1, 3, 5 and 7 days after the nutritional support. PBMCs were isolated and used for detection of the mRNA and protein expression of TLR2 and TLR4 by using real-time PCR and flow cytometry respectively, the levels of NF-κB by quantum dots-based immunofluorescence assay, the levels of TNF-α, IL-2, IL-6 and COX-2 by ELISA, respectively. The results showed that the mRNA and protein expression of TLR2 and TLR4 in PBMCs was significantly lower in ω-3PUFA group than in control group 5 and 7 days after nutrition support (both P<0.05). The levels of TNF-α, IL-2, IL-6 and COX-2 were found to be substantially decreased in PBMCs in ω-3PUFA group as compared with control group at 5th and 7th day (P<0.05 for all). It was concluded that ω-3PUFA can remarkably decrease the expression of TLR2, TLR4 and some related inflammatory factors in NF-κB signaling pathway in PBMCs of patients with severe multiple trauma, which suggests that ω-3PUFA may suppress the excessive inflammatory response meditated by the TLRs/NF-κB signaling pathway.

The Health Effect of the Number of Children on Chinese Elders: An Analysis Based on Hukou Category.

Based on the 2018 China Health and Retirement Longitudinal Study (CHARLS 2018), from the perspective of urban-rural disparity, this paper investigates how fertility affects Chinese elders' health. We exploit the enactment of the one-child policy in 1979 to construct instrumental variables capturing the health effect of having only one child rather than multiple children. The empirical results show that the health condition of rural elders having only one child is worse than elders having multiple children, while the negative health effect of lower fertility becomes statistically insignificant for urban elderly parents. After considering the selection on both levels and gains, the results are still robust in marginal treatment effect (MTE) estimation. We investigate the potential mechanism in four ways, the results suggest that having only one child instead of multiple children depresses the upstream intergenerational transfer payments more for rural parents; ameliorates offspring's educational attainment more for urban parents; improves housing conditions more for urban elders; and decreases the visit frequency of children to both urban and rural parents. Our findings have important implications, in the context of increasing population aging, the urban-rural inequality caused by the hukou system has been magnified by the declining fertility rate. The Chinese government should pay more attention to rural elders with only one child, and more public-funded socioeconomic resources are needed for one-child parents in rural areas to improve their health. Moreover, the empirical results also imply that urbanization in China may be able to soften the health deterrent effect of lower fertility.

The Relationship between Internet Use and Health among Older Adults in China: The Mediating Role of Social Capital.

A growing academic attention has been paid to the health effects of Internet use among older adults. However, the relationship between Internet use and health among older adults in China remains to be studied further. On the one hand, existing research is still controversial on this issue. On the other hand, the underlying mechanism of how Internet use affects the health of older adults has not been fully explored. This article examined the relationship between Internet use and health among older adults with the mediating role of social capital in China based on the 2018 wave of China Health and Retirement Longitudinal Study (CHARLS). This study reveals that Internet use has a positive association with the health of older adults, and the positive effects of internet use among older adults are heterogeneous in age and residential location. In addition, this study also demonstrates that social capital plays a partial mediating role between Internet use and physical health among older adults. It is important for the government to take effective measures to expand Internet use and enhance social capital among older adults.

Does the Effect of Internet Use on Chinese Citizens' Psychological Well-Being Differ Based on Their Hukou Category?

This paper draws support from the 2018 wave of the China Family Panel Studies (CFPS 2018) and uses unconditional quantile regression, re-centered influence function (RIF) decomposition, linear structural equation modelling, extended regression modelling and censored regression to explore the heterogeneity of the impact of Internet use on the psychological well-being of Chinese non-agricultural and agricultural hukou holders. We find that Internet use better improves the psychological well-being of non-agricultural hukou holders, thereby widening the gap in psychological well-being between urban and rural residents in China. Through RIF decomposition, we observe that, except for the 10th quantile, the expansion effect of Internet use on the inequality in psychological well-being between agricultural and non-agricultural hukou holders is mainly reflected in the structure effect, which shows that compared to non-agricultural hukou holders, the return rate of Internet use on the psychological well-being of agricultural hukou holders is lower. Further mechanism analysis shows that using the Internet to socialize, obtain information and understand politics is more beneficial for the psychological well-being of non-agricultural hukou holders; moreover, Internet use can further exert different effects on the psychological well-being of the two groups by differently influencing their job satisfaction, government evaluation, and sleep quality. This study also confirms that relying only on external scientific and technological progress has a limited corrective effect on existing inequalities.

Does Educational Attainment Affect Residents' Health?

Based on the data of the Chinese General Social Survey 2015 (CGSS2015), this article conducts an empirical analysis on the relationship between education and health status of Chinese residents by using the structural equation model (SEM), the propensity score matching (PSM) method, and generalized ordered logit (Gologit) model. Our study found that education promotes both the subjective and objective health of residents, and the finding holds true after considering the selection bias. In addition to having a direct role, education could promote health through improved mental health, economic status, and healthy behaviors. The finding is consistent with the explanations in existing research of "efficiency-improving effect", "mental health effect", and "budget relaxation effect". Further research on the mechanism of education affecting health through structural equation modeling finds that mental health plays a more important role than healthy behaviors and economic status. In terms of the differences of various groups, education has stronger effect on vulnerable groups with fewer social resources, which shows that education helps reduce health inequality. The conclusion has important policy significance.

LncRNA MBNL1-AS1 represses cell proliferation and enhances cell apoptosis via targeting miR-135a-5p/PHLPP2/FOXO1 axis in bladder cancer.

LncRNAs have been shown to play essential roles in bladder cancer (BC) progress. Our microarrays of clinical samples firstly screened that lncRNA muscleblind-like 1 antisense RNA 1 (MBNL1-AS1) was poorly expressed in BC tissues. However, its biological function in BC remains not well understood. Here we examined the clinical correlations with MBNL1-AS1 in BC patients. Then, 5673 and T24 cell lines were employed to investigate the role of MBNL1-AS1 in the proliferation and apoptosis of BC cells in vitro and in vivo. Furthermore, miR-135a-5p (miR-135a)/PHLPP2/FOXO1 axis was focused to explore its regulatory mechanism in BC. The results showed that MBNL1-AS1 was significantly downregulated in bladder tumor tissues, and associated with BC progression. In vitro, MBNL1-AS1 knockdown increased the number of viable cells and bromodeoxyuridine-positive cells, accelerated cell cycle, and dysregulated proliferative regulators (Ki67, p21, p27, and Cyclin D1) in BC cells. The apoptotic cells and the cleavages of caspase-3/9 were reduced in MBNL1-AS1-silenced BC cells. Overexpression of MBNL1-AS1 had opposite effects on BC cell proliferation and apoptosis. Moreover miR-135a was demonstrated to interact with MBNL1-AS1, and inhibiting miR-135a reversed the effects of shMBNL1-AS1 on BC cells. The downstream effectors (PHLPP2 and FOXO1) were positively regulated by MBNL1-AS1, but negatively regulated by miR-135a. Similar results were also observed in xenograft tumors. In conclusion, this study firstly suggests that MBNL1-AS1 acts as a tumor suppressor of BC by targeting miR-135a/PHLPP2/FOXO1 axis, providing a novel insight for BC diagnosis and treatment.

MiR-362-5p, Which Is Regulated by Long Non-Coding RNA MBNL1-AS1, Promotes the Cell Proliferation and Tumor Growth of Bladder Cancer by Targeting QKI.

In this study, we found miR-362-5p was upregulated in bladder cancer tissues and we predicted that QKI is potential a target of miR-362-5p and MBNL1-AS1 might be able to directly target to miR-362-5p. We attempted to evaluate whether miR-362-5p could play its roles in bladder cancer through regulating QKI (quaking) and whether the expression and function of miR-362-5p could be mediated by lncRNA MBNL1-AS1. We performed the gain- and loss-function experiments to explore the association between miR-362-5p expression and bladder cancer proliferation. In vivo, the nude mice were injected with miR-362-5p knockdown SW780 cells to assess the effects of miR-362-5p on tumor growth. The results showed upregulation of miR-362-5p promoted cell proliferation of bladder cancer cells. MBNL1-AS1 and QKI could directly bind with miR-362-5p, and knockdown of MBNL1-AS1 or QKI could abrogate the regulatory effects of miR-362-5p on bladder cancer cell proliferation. Furthermore, downregulation of miR-362-5p inhibited bladder tumor growth and increased QKI expression. Our data unveiled that miR-362-5p may play an oncogenic role in bladder cancer through QKI and MBNL1-AS1 might function as a sponge to mediate the miR-362-5p expression and function.

MiR-210-3p inhibits the tumor growth and metastasis of bladder cancer via targeting fibroblast growth factor receptor-like 1.

Current evidence indicates that microRNAs are widely down-regulated in various tumors including colorectal carcinoma, liver cancer and lung cancer, and function as tumor suppressors through inhibiting cancer cell growth, invasion and migration. Here, we demonstrated that miR-210-3p level was significantly reduced in the bladder cancer compared to paratumor tissues, and attempt to reveal the regulatory role of miR-210-3p in bladder cancer progression. Exogenous overexpression of miR-210-3p inhibited the proliferation, migration and invasion of bladder cancer cells in vitro. In addition, the nude mouse xenograft model showed that miR-210-3p over-expressing inhibited bladder cancer growth and liver metastasis whereas silencing miR-210-3p caused an opposite outcome, which is mainly regulated by targeting fibroblast growth factor receptor-like 1 (FGFRL1). We also demonstrated that the expression of FGFRL1 in bladder cancer specimens were negatively correlated with miR-210-3p level, and FGFRL1 overexpression rescued the cell proliferation and invasion inhibited by ectopic expression of miR-210-3p. Moreover, knockdown of FGFRL1 was able to mimic the cell growth and metastasis effects induced by miR-210-3p over-expressing in bladder cancer cells. Together, these results indicate that miR-210-3p plays an important role in the regulation of bladder cancer growth and metastasis in vitro and in vivo through targeting FGFRL1.

Effect of ω-3 Polyunsaturated Fatty Acid on Toll-like Receptors in Patients with Severe Multiple Trauma / 华中科技大学学报（医学）（英德文版）

This study examined the effects of ω-3 polyunsaturated fatty acid (ω-3PUFA) on the expression of toll-like receptor 2 (TLR2),toll-like receptor 4 (TLR4) and some related inflammatory factors in peripheral blood mononuclear cells (PBMCs) of patients with early-stage severe multiple trauma.Thirty-two patients who were admitted to the Department of Traumatic Surgery,Tongji Hospital (Wuhan,China) between May 2010 and November 2010,and diagnosed as having severe multiple trauma with a injury severity score (ISS) no less than 16,were enrolled in the study and divided into two groups at random (n=16 in each):ω-3PUFA group and control group in which routine parenteral nutrition supplemented with ω-3PUFA or not was administered to the patients in two groups for consecutive 7 days.Peripheral blood from these patients was collected within 2 h of admission (day 0),and 1,3,5 and 7days after the nutritional support.PBMCs were isolated and used for detection of the mRNA and protein expression of TLR2 and TLR4 by using real-time PCR and flow cytometry respectively,the levels of NF-κB by quantum dots-based immunofluorescence assay,the levels of TNF-α,IL-2,IL-6 and COX-2 by ELISA,respectively.The results showed that the mRNA and protein expression of TLR2 and TLR4 in PBMCs was significantly lower in ω-3PUFA group than in control group 5 and 7 days after nutrition support (both P＜0.05).The levels of TNF-α,IL-2,IL-6 and COX-2 were found to be substantially decreased in PBMCs in ω-3PUFA group as compared with control group at 5th and 7th day (P＜0.05 for all).It was concluded that ω-3PUFA can remarkably decrease the expression of TLR2,TLR4 and some related inflammatory factors in NF-κB signaling pathway in PBMCs of patients with severe multiple trauma,which suggests that ω-3PUFA may suppress the excessive inflammatory response meditated by the TLRs/NF-κB signaling pathway.