Differential expression and significance of CD4+ CD25+ Foxp3+ regulatory T cell in liver of arsenic-exposed rats
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Abstract:
Objective
To observe the differential expression level of CD4+ CD25+ Foxp3+ regulatory T cells (Treg) in liver of arsenic-exposed rats, explore the regulatory mechanisms on immunological of hepatic injury induced by arsenic, and provide a basis for prevention and treatment of the disease.
Methods
Thirty-two healthy Wistar rats were selected and randomly divided into control, low, medium and high arsenic dose groups by weight, 8 rats per group. Rats in control group were given oral gavage of deionized water, while the other groups were given oral gavage doses of 2.00 g/L sodium arsenite (NaAsO2) according to their body weight for 6 days every week, the concentrations were 1.25, 2.50 and 5.00 ml/kg. After 4 months, liver tissue samples of rats were collected, the content of arsenic in liver was detected by inductively coupled plasma mass spectrometry (ICP-MS); the expression of Treg cells in liver was detected by immunohistochemistry; enzyme-linked immunosorbent assay (ELISA) was applied to detect the levels of interloukin-10 (IL-10), transforming growth factor beta 1 (TGF-β1), IL-6, IL-17 and IL-2.
Results
Compared with the control group [28.57 (17.64-35.64) μg/g], the content of arsenic in liver in low, medium and high arsenic exposed groups [M (P25-P75): 638.30 (527.91-802.58), 591.64 (513.82-723.16), 792.55 (695.93-1 074.41) μg/g] increased, the differences were statistically significant (P 0.05); compared with control group [(16.30 ± 3.98) μg/L], the expression of IL-2 in high arsenic exposed group decreased [(9.93 ± 2.65) μg/L, P < 0.05]. The content of arsenic in liver was positively correlated with the expression of IL-10, TGF-β1, IL-17, IL-6 (rs= 0.696, 0.463, 0.632, 0.502, P < 0.05), and negatively correlated with the expression of IL-2 (rs=-0.522, P < 0.05).
Conclusion
With increasing of arsenic exposure level, the content of arsenic in liver and the expression of CD4+CD25+ Foxp3+ Treg have increased, the cytokines are secreted abnormally, liver immunological micro environment is disordered, immune tolerance is formed, and immune clearance is inhibited, which may play an important role in the occur and development of immunological liver damage induced by arsenic in rat.
Key words:
Arsenic; Regulatory T cells; Liver injury; ImmunosuppressionKeywords:
Sodium arsenite
Arsenic poisoning
Arsenic toxicity
Objective To observe the expression of Bcl-2,Bax and proliferating cell nuclear antigen(PCNA) in liver of rats with hepatic fibrosis and the effects of transforming growth factor (TGF)-β1 vaccine on them.Methods Thirty healthy male Sprague-Dawley rats were assigned into 3 groups,named healthy control group(n=10),hepatic fibrosis group(n=10) and TGF-β1 vaccine treated group(n=10).The animal model with hepatic fibrosis was established by injecting solution dimethylnitrosamine (DMN) into abdominal cavity with concentration as 0.5% and dose as 0.2 mL/ 100 g.In TGF-β1 vaccine treated group,every rat was not only injected with DMN but also 150μg TGF-β1 vaccine protein.On the 42nd day,all rats were sacrificed.Then the blood and the liver tis- sues were collected.The expression levels of Bcl-2,Bax and PCNA in liver tissues were detected by S -P immunohistochemistry and observed by routine pathological evaluation.Alanine aminotransferase (ALT),aspartate aminotransferase(AST) and albumin(Alb) were determined by auto biochemical analytical tool.Serum levels of hyaluronic acid (HA),laminin(LN) were detected by radioimmunoas- say (RIA).Results The expression of Bax,which promoted apoptosis,directly correlated with pathological grade in liver of rats,while the expression of Bcl-2 and Bcl-2/Bax,which protected a gainst apoptosis,inversely correlated with pathological grade in liver of rats.The expression levels of TGF-β1 and Bax in healthy control group were significantly lower than those of fibrosis group,how ever,the expression levels of Bcl-2 were comparable between these two groups.As compared with fi- brosis group,the expression of TGF-β1 was significantly lower while the expression of Bcl-2 was sig nificantly higher in TGF-β1 vaccine treated group.However,the expression of Bax was comparable between these two groups.The expression level of PCNA of fibrosis group was significantly higher than that of healthy control group but dramatically lower than that of TGF-β1 vaccine treated group (Both P0.01).Conclusions Hepatocyte apoptosis may be one mechanism for liver fibrosis devel- opment.TGF-β1 vaccine may influence the hepatocyte apoptosis and proliferation by affecting the ex- pression of Bcl-2,Bax and PCNA,which will contribute to the improvement of hepatic patbological grade.
Hepatic fibrosis
Bcl-2-associated X protein
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Objective
To investigate the effects of CD24 on CCl4-induced murine liver fibrosis and to analyze the possible molecular mechanism.
Methods
Wild type (WT) and CD24 knockout (CD24-/-) C57BL/6 mice were treated with CCl4 through intraperitoneal injection. Levels of ALT in serum samples were detected and liver tissues were stained with hematoxylin and eosin (HE) to assess liver tissue injury. Sirius Red staining was used to observe liver fibrosis. Real-time PCR was performed to detect the expression of α-SMA (α-smooth muscle actin), Col1a1 (Collagen, typeⅠ, alpha 1), TGF-β1 (transforming growth factor-β1) and CD24 at mRNA level in liver tissues. Western blot was performed to analyze the expression of α-SMA and Col1a1 at protein level. Flow cytometry analysis was used to detect the macrophages in liver tissues. ELISA was used to detect the expression of TGF-β1 in the culture supernatants of M1 and M2 macrophages.
Results
The expression of CD24 at both mRNA and protein levels were up-regulated in mice with CCl4-induced liver fibrosis. HE staining showed that liver inflammation in CD24-/- mice was more severe than that in WT mice after treated with CCl4. Sirius Red staining of paraffin-embadded liver sections revealed that compared with WT mice, CD24-/- mice presented with more severe liver fibrosis. Moreover, α-SMA and Col1a1, indicators of liver fibrosis, in CD24-/- mice were significantly higher than those in WT mice. Flow cytometry analysis showed that murine hepatic macrophages significantly increased in CD24-/- mice than in WT mice following CCl4 treatment. Real-time PCR analysis also confirmed that significantly enhanced expression of TGF-β1 at mRNA level in liver tissues was observed in CD24-/- mice than in WT mice. TGF-β1 secreted in the culture supernatant of M2 macrophages derived from CD24-/- mice group was more than that of the WT mice group. No significant difference in TGF-β1 secretion in culture supernatant of M1 macrophages was observed between the two groups.
Conclusion
Taken together, these data suggest that CD24 plays an important role in attenuating CCl4-induced chronic inflammation and hepatic fibrosis in mice. The mechanism of CD24 in alleviating liver fibrosis might be through regulating intrahepatic macrophages, inhibiting the secretion of TGF-β1 by M2 macrophages and suppressing the activation of hepatic stellate cells.
Key words:
CD24; CCl4; Liver fibrosis; Macrophage; TGF-β1
Sirius Red
CD24
CCL4
Intraperitoneal injection
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To investigate whether CD31 could regulate paracetamol-induced liver injury, thereby providing a new direction for the prevention and treatment of drug-induced hepatitis.Wild-type (WT) mice were treated with acetaminophen (APAP) (250 mg/kg) or isodose of phosphate-buffered saline (PBS). 1, 3, 6 and 12 h after the treatment, the messenger RNA (mRNA) and protein expression level of CD31 in the liver of mice were determined by Real-time reverse transcription polymerase chain reaction (RT-PCR) and Western blotting, respectively. Once CD31 was confirmed to be involved in APAP-induced liver injury, the acute liver injury model in WT mice and CD31 gene deficient (CD31-/-) mice induced by APAP was established. Serum samples were collected at 8 and 24 h after APAP injection (250 mg/kg), and the activity of serum alanine aminotransferase (ALT) was measured. The liver tissues of mice were isolated and analyzed by hematoxylin and eosin (HE) staining. Meanwhile, mononuclear cells (MNCs) were isolated from the liver tissues of mice. The number of infiltrating macrophages and neutrophils was detected by flow cytometry, and the activation level of these cells was analyzed. The expression levels of proinflammatory cytokines in liver tissues, such as TNF-α, IL-1β, keratinocyte chemoattractant (KC), MCP-1 and IL-6, were determined by RT-PCR. The expression levels of cytokines in serum were detected by enzyme-linked immunosorbent assay (ELISA). Moreover, the protein expression levels of JNK, Caspase-3, and cytochrome P450 2E1 (CYP2E1) in liver tissues were detected by Western blotting.After APAP treatment, we found that WT mice were more sensitive to APAP-induced liver injury. The level of ALT in WT mice was significantly higher than that of CD31-/- mice, meanwhile, more necrotic or apoptotic cells were found in WT mice. Results also indicated that the expression levels of inflammatory cytokines, including KC, IL-1β, MCP-1 and IL-6, were significantly higher in WT mice. Meanwhile, the number of infiltrating macrophages and neutrophils in the liver tissues of WT mice were much more than that of CD31-/- mice.APAP-treated CD31-/- mice exhibited less liver injury when compared with WT mice. We also confirmed that CD31 was greatly involved in APAP-induced inflammatory response by promoting hepatic inflammatory and cell apoptosis, which might provide a new strategy for the prevention and treatment of drug-induced hepatitis.
Proinflammatory cytokine
CD31
Acetaminophen
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Objective To investigate the alterations in levels of neurofilament(NF) mRNA and cellular immunity in rats infected with Toxoplasma gondii. Methods Four-week old male SD rats were randomly divided into two groups with ten animals for each. The subjects in the experimental group were i.p. injected with 2×10~(10)/L toxoplasma tachyzoits 2 ml for each. Meanwhile, each rat in the control group was i.p. injected with NaCl 2 ml. After 9 weeks, mRNA levels of light molecular NF(NF-L), medium molecular NF(NF-M) and high molecular NF (NF-H) in cerebrum were determined by RT-PCR. The percentages of CD3~+, CD4~+, CD8~+ T lymphocytes were examined by means of flow cytometry, and the peripheral blood serum levels of IFN-γ, TNF-α, IL-4 were analyzed by ELISA. Results The mRNA levels of NF-L, NF-H in rat cerebrum(0.51±0.06,0.68±0.05) decreased than control group(0.79±0.03,0.76±0.05, t = 3.41,2.17, P 0.05) than control group(0.72±0.03). No significant changes were observed on the levels of CD4~+T lymphocytes[ (32.19±5.01)%] and CD8~+T lymphocytes[(20.06±2.28)%], compare with the control group[(35.82±3.71)%, (22.06±3.90)%, t=1.69,1.88, all P > 0.05]. The serum levels of IFN-γ[(6.03±0.16)ng/L], TNF-α[(18.05±1.93)ng/L], IL-4[(15.76±1.59)ng/L] in experimental rats were significantly higher than those in the controls[ (4.77±0.13), (9.54±1.57), (5.67±0.42)ng/L, t = 2.81, 2.74,2.63, all P < 0.05]. Conclusion Toxoplasma gondii infection can decrease NF subunit mRNA expression levels in rat brain tissue and increase serum levels of IFN-γ, TNF-α and IL-4.
Key words:
Toxoplasma; Brain; Neurofilament; T-lymphocyte subsets; Cytokines
Cellular immunity
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BACKGROUND The aim of this study was to study the effects of 1-alpha,25-dihydroxy-cholecalcifero (1,25(OH)2D3) on liver fibrosis and the generation of Th17 cells in vivo and in vitro. MATERIAL AND METHODS Thirty C57 mice were randomly divided into control, model, and treatment groups. Hepatic fibrosis was induced by subcutaneous injection of CCl4. Liver fibrosis condition was evaluated through pathological inspection and blood biochemical examination of liver function. Immunohistochemical assays were used to detect the expression of α-SMA, TGF-β, and collagen I to observe hepatic stellate cell activation level. Flow cytometry, ELISA, and RT-PCR were performed to explore the association between 1,25(OH)2D3 and Th17 cell differentiation. RESULTS Collagen I, TGF-β, and α-SMA were decreased after 1,25(OH)2D3 treatment. Consistently, RORγt mRNA and the rate of Th17 cells was significantly reduced after 1,25(OH)2D3 treatment. In vitro, the proportion of Th17 cells was also obviously reduced in the 1,25(OH)2D3 group, and mRNA levels of IL-17A, IL-22, RORγt, and RORa were significantly decrease in the 1,25(OH)2D3 group compared to the control group. CONCLUSIONS Treatment with 1,25(OH)2D3 can alleviate the damage caused by liver fibrosis. Experiments in vivo and in vitro showed that 1,25(OH)2D3 treatment deceased the rates of Th1 and Th17 cells and increased the rate of Th2 cells. The level of IL-17A, IL-22 and IFN-γ were decreased, while the level of IL-4 was increased by the treatment of 1,25(OH)2D3.
CCL4
Hepatic stellate cell
Hepatic fibrosis
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This study aims to explore the relationship between miR-195 and CD40 and its effect on Th17/Treg balance in rats with non-alcoholic fatty liver disease (NAFLD).We established rat models of NAFLD and made seven groups, Normal group (without modeling), Model group (model rats), NC group (model rats injected with negative control vector), miR-195 OE group (model rats injected with miR-195 mimic), anti-miR-195 group (model rats injected with miR-195 inhibitor), Si-CD40 group (model rats injected with CD40 silencing vector), and anti-miR-195+Si-CD40 group (model rats injected with miR-195 inhibitor and CD40 silencing vector). Dual-luciferase reporter gene assay verified the targeting relationship between miR-195 and CD40. The mRNA and protein expression levels of miR-195, CD40 as well as Th17/Treg associated cytokines in the liver tissues were detected. The pathological changes of liver tissues were detected, and the liver lesion scoring was carried out. The liver coefficient was calculated. The levels of liver function related indices, and Th17/Treg associated cytokines and inflammatory factors in serum were determined. The proportions of Th17/Treg cells in serum were determined by flow cytometry.Compared with Normal group, miR-195 expression level in liver tissues of rats in other six groups was significantly reduced (all P < 0.05); the serum levels of AST, ALT, GGT, IL-17, TNF-α, IL-23, IL-6, IL-8, TC, TG, HDL, and LDL, and the Th17/Treg ratio, as well as the mRNA and protein expression levels of CD40, RORyt, IL-17, TNF-α, IL-23, and IL-8 in liver tissues were significantly increased (all P < 0.05); while the mRNA and protein expression levels of Foxp3, and IL-10 level were significantly reduced (all P < 0.05). Compared with Model group, the above parameters showed an opposite trend in miR-195 OE group and Si-CD40 group were significantly reduced (all P < 0.05). Moreover, anti-miR-195 group could aggravate the imbalance of Th17/Treg cells in rats with NAFLD and promote inflammatory response. Compared with anti-miR-195 group, the combined treatment in anti-miR-195+Si-CD40 group can partially avoid the imbalance of Th17/Treg cells, and inhibit inflammatory response.Overexpression of miR-195 can reduce the Th17/Treg ratio to maintain Th17/Treg balance by inhibiting CD40 expression in rats with NAFLD.
Treg cell
Alcoholic fatty liver
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Objective To investigate the effect and mechanism of cyclooxygenase-2 (COX-2) on sodium arsenic-induced microglia activation in mice. Methods Twenty of C57BL/6J male mice were randomly divided into a control group supplied with tap water and an arsenic exposure group administered with drinking water containing 50 mg/L sodium arsenite (NaAsO 2 ) continuously for 12 weeks to establish a chronic arsenic exposure model. Morris water maze was used to test learning and memory ability of the mice. Hematoxylin-eosin (HE) staining and transmission electron microscopy were used to observe pathological changes of neuron and ultrastructure in hippocampus. Immunofluorescence microscopy was used to determine expression of ionized calcium-binding adapter molecule 1 (IBA-1) in hippocampus. The protein expressions of IBA-1, COX-2, transcription factor nuclear factor kappa-Bp65 (NF- κ Bp65) were detected with Western blot. The concentration of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF- α ) was measured with enzyme-linked immunosorbent assay (ELISA). Results Compared to the control group, the mice with arsenic exposure had significantly increased escape latency time (50.79 ± 12.30 vs. 29.01 ± 18.10 seconds) but decreased effectively traveled distance (9.34 ± 2.34 vs. 11.78 ± 1.25 centimeters) (both P < 0.05l). Pathological changes such as disarrangement of cells, edema and nuclei atrophy were observed in the hippocampus of arsenic exposed mice. The protein expression of IBA-1 was increased in arsenic exposed mice based on observation of green fluorescence aggregation with fluorescence microscope. In comparison with those in hippocampus of the control mice, significantly higher levels of IBA-1 (1.01 ± 0.12 vs. 0.75 ± 0.13), NF- κ Bp65 (1.23 ± 0.11 vs. 0.86 ± 0.14), COX-2 (1.14 ± 0.13 vs. 0.74 ± 0.12), IL-6 (93.61 ± 3.18 vs. 43.37 ± 1.11 pg/mL) and TNF- α (604.00 ± 25.02 vs. 198.46 ± 9.93 pg/mL) were detected in arsenic exposed mice ( P < 0.05 for all). Conclusion Chronic arsenic exposure-induced learning and memory impairment are associated with the activation of microglia by the activation of NF- κ B and the increase in the secretion of pro-inflammatory cytokines by upregulation of COX-2 in mice 【摘 要】 目的 探讨环氧合酶-2（COX-2）在亚砷酸钠诱导小鼠小胶质细胞活化中的作用及机制。 方法 建立慢性小鼠饮水砷暴露模型，将 20 只 C57BL/6J 雄性小鼠随机分为对照组（自来水）和砷暴露组（50 mg/L NaAsO 2 ），连续自由饮水暴露 12 周。Morris 水迷宫实验检测小鼠学习记忆能力；苏木精-伊红染色和透射电镜观察海马区神经元病理变化及超微结构改变；免疫荧光检测海马区离子钙结合配适分子-1（IBA-1）表达；蛋白印迹法（WB）检测海马区 IBA-1、COX-2、核因子 κ B p65（NF- κ B p65）蛋白表达；酶联免疫吸附法（ELISA）检测海马区白细胞介素-6（IL-6）和肿瘤坏死因子 α （TNF- α ）表达。 结果 与对照组小鼠[逃避潜伏期（29.01 ± 18.10）s、有效停留距离（11.78 ± 1.25）cm]比较，砷暴露组小鼠逃避潜伏期[（50.79 ± 12.30）s]延长，有效停留距离明显缩短[（9.34 ± 2.34）cm]（ P < 0.05）；砷暴露组小鼠海马区出现细胞排列紊乱、水肿、皱缩等病理改变，荧光显微镜下 IBA-1 绿色荧光表达增多。与对照组[IBA-1 （0.75 ± 0.13）、NF- κ B p65（0.86 ± 0.14）、COX-2（0.74 ± 0.12）表达水平及 IL-6（43.37 ± 1.11）pg/mL、TNF- α （198.46 ± 9.93）pg/mL 含量]比较，砷暴露组小鼠海马 IBA-1（1.01 ± 0.12）、NF- κ Bp65（1.23 ± 0.11）、COX-2（1.14 ± 0.13）表达水平及 IL-6 和 TNF-α 含量[分别为（93.61 ± 3.18）、（604.00 ± 25.02）pg/mL]明显升高，差异均具有统计学意义（ P < 0.05）。 结论 慢性砷暴露导致小鼠学习记忆损伤机制可能与小胶质细胞活化，激活 NF- κ B 上调 COX-2 分泌促炎性细胞因子，促进神经炎症有关。
Sodium arsenite
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The aim of this study was to investigate the expression of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) in juvenile rats with nephrotic syndrome, and to explore its effects on inflammatory changes and renal injury.24 Sprague-Dawley (SD) rats were randomly divided into the normal group (n=12) and model group (n=12). Rats in the normal group were intraperitoneally injected with normal saline. Meanwhile, rats in the model group were given azithromycin hydrochloride injection to establish the model of nephrotic syndrome. After 24 h of modeling, the samples were collected. The expression of NF-κB was detected via immunohistochemistry. Moreover, the protein expression of NF-κB was determined through Western blotting. Quantitative Polymerase Chain Reaction (qPCR) was used to measure the messenger ribonucleic acid (mRNA) expression levels of interleukin-1 (IL-1) and IL-6. Meanwhile, the content of IL-1 and IL-6 was detected by enzyme-linked immunosorbent assay (ELISA). The serum levels of urea nitrogen and serum creatinine were measured by an automatic biochemical analyzer. Furthermore, the correlation between NF-κB protein with IL-1 and IL-6 were studied via Pearson analysis.Compared with the normal group, rats in the model group exhibited significantly increased expression and protein expression of NF-κB (p<0.05). Meanwhile, the mRNA expression levels and content of IL-1 and IL-6 (p<0.05), as well as the serum levels of urea nitrogen and creatinine (p<0.05) of the model group were markedly higher than those of the normal group. Furthermore, NF-κB protein was positively correlated with IL-1 and IL-6 contents.NF-κB is highly expressed in juvenile rats with nephrotic syndrome, which promotes the expressions of inflammatory factors (IL-1 and IL-6) and aggravates the renal injury.
Blood urea nitrogen
Group A
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To investigate the regulatory effects of the Toll-like receptor 4 (TLR4) and the nuclear factor kappa-light-chain-enhancer of the activated B cells (NF-κB) on primary biliary cholangitis (PBC) and to analyze the possible mechanisms.A total of 24 C57BL/6 mice were randomly divided into M group (n=12, intraperitoneally injected with polyinosinic acid-polycytidine acid (PolyI:C) for 12 consecutive weeks, 2 times/week) and C group (n=12, intraperitoneally injected with the same volume of normal saline). After 12 weeks, the mice were sacrificed to collect liver tissues. Then, an enzyme-linked immunosorbent assay (ELISA) kit was used to detect the content of interleukin-6 (IL-6), IL-10, and tumor necrosis factor-alpha (TNF-α) in liver tissues. Hematoxylin-eosin (HE) staining assay was performed to observe the pathological changes of liver tissues, and measure the levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in peripheral blood of mice. Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end-labeling (TUNEL) staining was applied to determine cell apoptosis in liver tissues. The relative messenger ribonucleic acid (mRNA) expression levels of TLR4 and NF-κB in liver tissues were detected by quantitative Polymerase Chain Reaction (qPCR). Western blotting was adopted to measure the protein expressions of TLR4, NF-κB, myeloid differentiation factor 88 (MyD88), B-cell lymphoma 2 (Bcl-2)/Bcl-2-associated X protein (Bax), and Caspase-3.Compared with that in C group, the content of IL-6 and TNF-α in liver tissues in M group was significantly increased (p<0.01), but the level of IL-10 was statistically downregulated (p<0.01). According to HE staining, liver damage of mice in M group was evidently severer than that in C group, and the levels of ALT and AST in M group were significantly higher than those in C group (p<0.01). The amount of TUNEL-positive cells in liver tissues in M group was significantly greater than that in C group (p<0.01). The levels of TLR4 and NF-κB mRNA in liver tissues from M group were significantly elevated in comparison with the C group (p<0.01). Compared with those in C group, the expressions of TLR4, NF-κB, MyD88, and Caspase-3 proteins in M group showed statistical increases in liver tissues (p<0.01), whereas that of Bcl-2/Bax was significantly declined (p<0.01).PBC activates the TLR4/MyD88/NF-κB signaling pathway, induces the release of inflammatory factors and produces a large number of apoptotic proteins, which results in liver damage and cell apoptosis in mice.
Terminal deoxynucleotidyl transferase
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Objective To investigate the effects of traumatic stress on cell immunity of mice amputee model, and the influences of Astragalus polysaccharide (APS) on the cell immunity. Methods 50 BALB/c mice were divided randomly into 5 groups: group A (normal control group), group B (traumatic stress group), group C(traumatic stress + high dose APS group), group D(traumatic stress + middle dose APS group) and group E(traumatic stress+low dose APS group). The groups A and B were given 0.5ml of normal saline by interaperitoneal injection daily, and the groups C, D and E were given 1000mg/kg, 500mg/kg and 250mg/kg of APS by interaperitoneal injection daily for three days. CD4+, CD8+ and expression of c-fos protein were detected by immunohistochemisty method. Expression of NF-κB mRNA and IL-10 mRNA were detected by hybridization in situ. Their results were quantitated by HPIAS-1000 system. Results Compared with group A, in thymus and spleen tissues, the expression level of NF-κB mRNA, IL-10 mRNA and the distribution of c-fos antigen of group B were elevated significantly (P0.01), CD4+ and CD4+/CD8+ were reduced(P0.01). Compared with group B, the level of expression of NF-κB mRNA and IL-10 mRNA in thymus and spleen tissues were not only depressed by APS and the level of CD4+ antigen, CD4+/CD8+ ratio were elevated in groups C, D and E; but the level of c-fos antigen were reduced(P0.01). The expression of NF-κB mRNA and IL-10 mRNA, CD4+ and CD4+/CD8+ and the distribution of c-fos antigen had no significant difference in both groups A and C (P0.05). Conclusion The cell immunity function of mice were disordered after their trauma, APS may play a role in restoring cell immunity.
Group A
Astragalus
Cellular immunity
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