To explore the expression and clinical significance of molecular chaperone heat shock protein 90 (HSP90) in peripheral blood mononuclear cells (PBMC) and plasma level of interleukin-6 (IL-6) in patients with systemic lupus erythematosus (SLE), HSP90 was detected in PBMC by Western blot assay and the plasma level of IL-6 was measured by ELISA in 38 SLE patients and 20 normal controls. The correlation analysis was performed between the SLE disease activity index (SLE-DAI) and the expression of HSP90 and IL-6. The results showed that there was increased expression of HSP90 in the SLE patients. The active SLE group exhibited higher HSP90 levels (0.82+/-0.10) than the inactive SLE group (0.54+/-0.09) (P<0.01). The expression of HSP90 in normal control group (0.37+/-0.11) showed significant statistical difference as compared to both the inactive and active SLE groups (P<0.01, P<0.01, respectively). The plasma level of IL-6 exhibited a significant increase in both the inactive and active SLE groups (28.99+/-1.74 pg/mL, 44.58+/-9.15 pg/mL, respectively) compared with normal control group (P<0.01, P<0.01, respectively). The expression of HSP90 and IL-6 in SLE patients showed significant positive correlation with SLEDAI scoring (r=0.80, P<0.01: r= 0.74, P<0.01, respectively). In addition, there was a positive correlation between the level of IL-6 and HSP90 in SLE patients (r=0.86, P<0.01). The increased expression of molecular chaperone HSP90 and IL-6 may play an important role in the pathogenesis of SLE by regulating autoimmunity.

Objective To investigate the mRNA expression of a proliferation inducing ligand (APRIL) and its receptors including B cell maturation antigen (BCMA),transmembrane activator.calcium modulator and cyclophilin ligand interactor (TACI) in the peripheral blood mononuclear cells (PBMCs) of patients with systemic lupus erythematosus (SEE).Methods APRIL mRNA、BCMA mRNA and TACI mRNA in PBMCs were detected by real-time quantitative PCR in 66 SLE patients and 25 normal controls.Gene expression level was measured as 2-AACT.Results The expression levels of APRIL mRNA、BCMA mRNA and TACI-mRNA were significantly increased in both active SLE group and stable SLE group compared with those in the normal controls(P<0.01 for all).The expression levels of APRIL mRNA and TACI mRNA in active SLE group were significantly higher than those in stable SLE group(P<0.01,P<0.05,respectively).But there was no significant difierence in the expression levels of BCMA mRNA between the SLE stable and active groups-Beside,the expression levels of APRIL mRNA and TACI mRNA were significantly increased in patients with lupus nephritis (LN) compared to patients with non-LN (P<0.01 for all).Conclusion The expression levels of APRIL and its receptors are significantly elevated in SLE patients.It may suggest that APRIL and its receptors play an important role in the pathogenesis of SLE.

To explore the expression and clinical significance of molecular chaperone heat shock protein 90 (HSP90) in peripheral blood mononuclear cells (PBMC) and plasma level of interleukin-6ells (PBMC) and plasma level of interleukin-6(IL-6) in patients with systemic lupus erythematosus (SLE), HSP90 was detected in PBMC by West and the plasma level of IL-6 was measured by ELISA in 38 SLE patients and 20 normal controls. The correlation analysis was performed between the SLE disease activity index (SLEe results showed that there was increased expression of HSP90 in the SLE patients. The active SLE group exhibited higher HSP90 levels (0.82±0.10) than group (0.54±0.09) (P＜0.01). The expression of HSP90 in normal control group (0.37±0. 11) showed significant statistical difference as compared to both the inactive and active SLE The plasma level of IL-6 exhibited a significant increase in both the inactive and active SLE groups (28.99±1.74 pg/mL, 44.58±9.15 pg/mL, respectively) com0.01, P＜0.01, respectively). The expression of HSP90 and IL-6in SLE patients showed significant positive correlation with SLEDAI scoring (r=0.80, P＜0.01: r=. In addition, there was a positive correlation between the level of IL-6 and HSP90 in SLE patients (r= 0.86, P＜0.01). The increased expression of molecular chaperone HSP90thogenesis of SLE by regulating autoimmunity.

Summary: CD4+CD25+ regulatory T cells (Tregs) and the expression of their molecular markers (GITR, Foxp3) in peripheral blood of the patients with systemic lupus erythematosus (SLE) were investigated in order to reveal the pathogenesis of SLE on the cellular and molecular levels. The level of Tregs in peripheral blood was detected by flow cytometry. The expression levels of GITR and Foxp3 mRNA in peripheral blood mononuclear cells (PBMCs) were assayed by reverse transcriptasepolymerase chain reaction (RT-PCR). The level of IL-6 in the plasma was measured by ELISA.Comparisons were made among 3 groups: the active SLE group, the inactive SLE group, and normal control group. The level of Tregs in the active SLE group and the inactive SLE group was significantly lower than in the normal control group (P<0.01). The level of Tregs in the active group was lower than in the inactive group with the difference being not significant (P>0.05). The level of Tregs in SLE patients was significantly negatively correlated with the disease active index in SLE (SLEDAI) (r=--0.81, P<0.01). The expression levels of GITR mRNA in PBMCs of the active SLE group and the inactive SLE group were significantly higher than in the normal control group (P<0.05), and those of Foxp3 mRNA in SLE patients of both active and inactive SLE groups were significantly lower than in the normal control group (P<0.05). There was no significant difference in the expression of GITR and Foxp3 mRNA between the active SLE group and inactive SLE group (P>0.05). The plasma levels of IL-6 in both the inactive SLE group and active SLE group were significantly higher than in the normal control group (P<0.01). The plasma level of IL-6 in the active S LE group was significantly increased as compared with that in the inactive SLE group (P<0.05), and the plasma level of IL-6 in SLE was significantly positively correlated with SLEDAI scores (r=0.58, P<0.01) and significantly negatively correlated with the ratio of CD4+CD25+ cells/CD4+ cells (r=-0.389, P<0.05). It was concluded that the levels of Tregs and Foxp3 mRNA in peripheral blood of SLE patients were decreased and the levels of GITR mRNA and plasma IL-6 were increased. The Tregs and their molecular markers GITR, Foxp3 as well as the plasma IL-6 might play an important role in the pathogenesis of SLE.

Glucagon like peptide-1(GLP-1) is a category of peptide secreted by intestine. The finding of GLP-1 was originated from the observation of "Incretin" phenomenon in 1960s. Besides lowering plasma glucose, GLP-1 can protect pancreas,improve cardiovascular outcome,and play a role in regulating appetite,as well as lower body weight. Given that food intake regulation mechanism modulated by GLP-1 remains uncertain,it is postulated that the central nervous system has played a vital role in this mechanism. In the present review,we focused on the following aspects about central nervous system's role in GLP-1's regulation of appetite:(1)The brain nuclei related to appetite regulation;(2) The brain nuclei related to blood glucose regulation; (3) The brain nuclei related to food intake reward behavior;(4) the role of food-related peptides and GLP-1;(5) How the GLP-1 receptor expression nuclei regulates the food intake.

Background::The causal relationship between visceral adipose tissue (VAT) and gout is still unclear. We aimed to examine the potential association between them using observational and Mendelian randomization (MR) analyses.Methods::In the observational analyses, a total of 11,967 participants (aged 39.5 ± 11.5 years) were included from the National Health and Nutrition Examination Survey. Logistic regression models were used to investigate the association between VAT mass and the risk of gout. In two-sample MR analyses, 211 VAT mass-related independent genetic variants (derived from genome-wide association studies in 325,153 UK biobank participants) were used as instrumental variables. The random-effects inverse-variance weighted (IVW) method was used as the primary analysis. Additional sensitivity analyses were also performed to validate our results.Results::Observational analyses found that an increase in VAT mass (per standard deviation) was associated with a higher risk of gout after controlling for confounding factors (odds ratio [OR] = 1.27, 95% confidence intervals [CI] = 1.11–1.45). The two-sample MR analyses demonstrated a causal relationship between increased VAT mass and the risk of gout in primary analyses (OR = 1.78, 95% CI = 1.57–2.03). Sensitivity analyses also showed similar findings, including MR-Egger, weighted median, simple mode, weighted mode, and leave-one-out analyses.Conclusions::Observational analyses showed a robust association of VAT mass with the risk of gout. Meanwhile, MR analyses also provided evidence of a causal relationship between them. In summary, our findings suggested that targeted interventions for VAT mass may be beneficial to prevent gout.

The pathogenesis of diabetic nephropathy(DN)is very complex.Ferroptosis as a kind of new way of cell death has become a research hotspot in recent years.It is widely known that DN is closely related to ferroptosis.Deactivation of system Xc--GSH-GPX4 axis,iron overload,lipid peroxidation and mitochondrial dysfunction play important role in occurrence and development of ferroptosis of DN,antioxidant protein may be a potential target for the treatment of ferroptosis of DN.Different pathways and interactions may alleviate the occurrence and development of ferroptosis by activating antioxidant protein such as GPX4,Nrf2,Sirtuin family protein and ferritin.Traditional Chinese medicine(TCM)has the characteristics of multi-component,multi-target and multi-pathway overall regulation.The active components and compounds of TCM have potential application value in improving renal injury and ferroptosis of DN by enhancing the expression of antioxidant protein,which provides a new research direction for delaying the progress of DN.

Iron is indispensable for the viablility of nearly all living organisms, and it is imperative for cells, tissues, and organisms to acquire this essential metal sufficiently and maintain its metabolic stability for survival. Disruption of iron homeostasis can lead to the development of various diseases. There is a robust connection between iron metabolism and infection, immunity, inflammation, and aging, suggesting that disorders in iron metabolism may contribute to the pathogenesis of arthritis. Numerous studies have focused on the significant role of iron metabolism in the development of arthritis and its potential for targeted drug therapy. Targeting iron metabolism offers a promising approach for individualized treatment of arthritis. Therefore, this review aimed to investigate the mechanisms by which the body maintains iron metabolism and the impacts of iron and iron metabolism disorders on arthritis. Furthermore, this review aimed to identify potential therapeutic targets and active substances related to iron metabolism, which could provide promising research directions in this field.