Objective To evaluate the cardiovascular disease (CVD) risk of the patients with metabolic syndrome (MS) by CVD predictive models. Methods The CVD risk of MS patients (n=637) and type 2 diabetes mellitus (T2DM)(n=259) were assessed by Framingham and ischemia CVD (ICVD) predictive models. The technique of myocardial nuclide development (MCND) was used on 121 MS patients to confirm the evaluation. Results The CVD risk of MS patients was significantly higher than that of T2DM. The proportion of CVD risk ≥ 5% in MS group was significantly higher than that in T2DM group. An elevated tendency of the proportion of CVD risk ≥ 10% appeared followed the age increasing in both MS and T2DM groups. The proportion of CVD risk ≥ 5% in male patients was higher than that in females assessed by Framingham predictive model, while an opposite result was given by ICVD predictive model. The MCND findings showed that, the more the increasing of CVD risk evaluated by Framingham predictive model,the severer the myocardial ischemia was. Conclusions The CVD risk of patients with MS is significantly higher than that of T2DM assessed by the both models. Framingham model is more susceptible to predicate CHD in MS patients than ICVD model.

Objective To observe the effects of Slit2 protein on the proliferation and migration of VSMCs .Methods The VSMCs was cultured in our laboratory .The experiment was divided into two parts ,part one:VSMCs were divided into normal con‐trol group and experimental groups(culture with 50 ,75 ,100 ,125 and 150 ng/mL Slit2 respectively);part two :VSMCs were divided into normal control group ,positive control group(culture with TNF‐α10 ng/mL) and experimental groups(culture with TNF‐α10 ng/mL+Slit2 50 ng/mL ,TNF‐α10 ng/mL+Slit2 75ng/mL ,TNF‐α10 ng/mL+ Slit2 100 ng/mL ,TNF‐α10 ng/mL+ Slit2 125 ng/mL and TNF‐α10 ng/mL+Slit2 150 ng/mL respectively) .To detect proliferation and migration of VSMCs by CCK‐8 and tran‐swell experiment .Results The difference of OD value and numbers of VSMCs has no statistical significance in the presence of Slit 2 (P=0 .516 ,P=0 .52) .The numbers of VSMCs has statistical significance between control and positive control groups (P=0 .00) . The numbers of VSMCs in experimental groups were fewer than positive control group (P<0 .05) ,whereas the difference of OD value still has no statistical significance between experimental and positive groups (P= 0 .173) .Conclusion Recombinant Slit2 could inhibits migration in VSMCs induced by TNF‐α,whereas it has no effect on proliferation of VSMCs .

Objective To observe the effect of atorvastatin on intraabdominal fat and microalbuminuria (MAU) in patients with metabolic syndrome (MS). Methods Forty-four MS patients were divided into the atorvastatin group and the control group. Blood pressure and blood glucose were controlled in both groups, in addition, atorvastatin was administered to the patients in the atorvastatin group. Blood pressure, blood glucose, body weight, abdominal wall fat, intraabdominal fat and MAU were compared before and after 12 weeks’ treatment. Results Obvious decrease of the intraabdominal fat and MAU was found in the atorvastatin group compared with those before the treatment Intraabdominal fat: non-ACE1/ARB (41.76?3.61) mm vs (33.23?2.47) mm, P

Genetically engineered intestinal microbes could be powerful tools to detect and treat intestine inflammation due to their non-invasive character, low costs, and convenience. Intestinal inflammation is usually detected along with an increasing concentration of thiosulfate and tetrathionate molecules in the intestines. ThsSR and TtrSR are two-component biosensors to detect the presence of thiosulfate and tetrathionate molecules, respectively. In real-life intestinal inflammation detection, sophisticated instruments are needed if using fluorescent proteins as reporters. However, chromoproteins and other colored small molecules, which can be seen by the unaided eye, could extend the use of ThsSR and TtrSR biosensors to detect intestine inflammation. The feasibility of ThsSR and TtrSR systems was tested by monitoring the fluorescence intensity of sfGFP in response to the concentration of thiosulfate and tetrathionate, followed by the incorporation of the two systems into Escherichia coli Top10 and E. coli Nissle 1917. The potential for the real-life application of the two systems was further corroborated by substituting sfGFP with a series of chromoproteins and a protoviolaceinic acid synthesis cassette as reporter genes. The results indicated that signal expression of the new systems had a positive correlation with the concentration of tetrathionate and thiosulfate molecules. Thus, the modified ThsSR and TtrSR system may potentially be applied in the human body for the detection of intestinal inflammation.
Escherichia coli ; Humans ; Inflammatory Bowel Diseases ; Intestines ; Thiosulfates

OBJECTIVE To explore the action mechanism of kushenol F （KSCF） in treating ulcerative colitis （UC） in mice. METHODS The potential targets of KSCF intervening in UC were predicted with network pharmacology and molecular docking. C57BL/6J mice were randomly divided by body weight into model group， positive control group （sulfasalazine， 703 mg/kg）， KSCF group （100 mg/kg）， and normal group， with 6 mice per group. The UC model of mice was induced by dextran sulfate sodium solution. During the modeling period， the mice were given relevant medicine intragastrically， once a day， for 7 consecutive days. After the last administration， the disease activity index （DAI） of the mice was scored； the length of the mice’s colon was measured； pathological changes in the colon tissue of mice were observed； the levels of lipopolysaccharide （LPS） in serum， myeloperoxidase （MPO）， nitric oxide （NO） and superoxide dismutase （SOD） in the colon were detected in mice； the expression levels of occludin and ZO-1 in colon tissue of mice were detected； the proportions of CD3+T， CD4+T， and CD8+T lymphocytes in the spleen and the ratio of CD4+/CD8+ were detected； changes in colonic microbiota were analyzed by 16S rDNA sequencing. RESULTS Results of network pharmacology indicated that KSCF may treat UC by regulating signaling pathways such as phosphatidylinositol-3 kinase/protein kinase B （PI3K/AKT） and nuclear factor kappa B （NF- κB）. Molecular docking results showed that KSCF bound most stably with NF-κB p65 protein. Animal experiment results demonstrated that， compared with the model group， the pathological characteristics of colon tissue in mice were improved in KSCF group. DAI scores， serum levels of LPS， the levels of MPO，NF-κB p65 phosphorylation and NLRP3 protein expression in the colon， and the proportion of CD8+T lymphocytes in the spleen were reduced significantly （P＜0.05）. Body weight， SOD levels， expression levels of occludin and ZO-1 in the colon， proportions of CD3+T and CD4+T lymphocytes， and the CD4+/CD8+ ratio in the spleen were significantly increased （P＜0.05）； the abundance of Firmicutes， Actinobacteria， Akkermansia， and Lactobacillus genera were increased， while Proteobacteria decreased； the microbial community structure tended towards that of the normal group. CONCLUSIONS KSCF alleviates UC by restoring intestinal microbial imbalance， enhancing immune response， and inhibiting colonic inflammatory responses， thereby improving intestinal barrier integrity.

OBJECTIVE To investigate the intervention effect of kushenol F （KSC-F） on ulcerative colitis （UC） mice. METHODS Totally 30 male C57BL/6J mice were randomly divided into the normal group， model group， positive drug group （sulfasalazine， 703 mg/kg）， KSC-F 50 mg/kg group （KSC-F50 group）， and KSC-F 100 mg/kg group （KSC-F100 group）， with 6 mice in each group. Except for the normal group， the mice in the remaining groups were given 3% dextran sulfate sodium solution continuously for 7 days to induce UC model. Concurrently， administration groups received corresponding drug solution intragastrically， once a day， for 10 consecutive days. During the experiment， the changes in body weight and bowel movements of the mice were observed. Disease activity index scoring was performed after the last administration. The histopathological morphology of colonic tissue was examined. The levels of inflammatory factors in the serum and colon tissue were measured. Additionally， the mRNA expression of inflammatory factors， and the protein expressions of inflammation-related proteins [interleukin-1β （IL-1β）， forkhead box O1（FOXO1）， phosphoinositide 3-kinase（PI3K）， phosphorylated PI3K（p-PI3K）， p38 mitogen-activated protein kinase（p38 MAPK）， phosphorylated p38 MAPK（p-p38 MPAK） and phosphorylated protein kinase B（p- Akt）] were determined in colonic tissue. RESULTS KSC-F could alleviate weight loss and colonic tissue damage in UC mice. KSC- F reduced the levels of IL-1β， IL-6， IL-8 and tumor necrosis factor-α （TNF-α） in serum， as well as IL-1β， IL-6， IL-17 and TNF- α in colonic tissue to varying degrees and increased the levels of IL-10 in both serum and colonic tissue （P＜0.05 or P＜0.01）. Moreover， KSC-F decreased the expression levels of IL-1β， IL-17 and TNF-α mRNA， as well as p-PI3K， p-p38 MAPK， and p- Akt proteins in colonic tissue to varying degrees， and increased the expression levels of IL-10 mRNA and FOXO1 protein in colonic tissue （P＜0.05 or P＜0.01）. CONCLUSIONS KSC-F effectively alleviates UC symptoms in mice by inhibiting PI3K， Akt and p38 MAPK activation， mitigating the release of pro-inflammatory factors such as IL-1β， IL-6， TNF- α，promoting the anti-inflammatory factor IL-10 secretion， and reducing inflammation-induced colonic tissue damage.