OBJECTIVE:To study the effect of alcohol extract of Toddalia asiatica on the inflammation-associated cytokines of model rats with adjuvant arthritis(AA). METHODS:70 SD rats were randomly divided into a normal control group,a model con-trol group,a positive control chemical medicine group(Leflunomide tablets,0.012 g/kg),a positive control TCM group(Tripter-ygium glycosides tablets,0.012 g/kg)and the groups of low,medium and high-dose [1,4,6 g(crude drug)/kg] alcohol extract of T. asiatica,with 10 rats in each group. The rats in all groups except for the normal control group were given complete Freund’s complete adjuvant id for the establishment of AA models. At the same time,the rats in the drug administration groups were given corresponding drugs ig,while those in the normal control group and the model control group were given isometric normal saline ig,twice a day,for 28 consecutive days. The degree of toe swelling,arthritis index and the levels of interleukin(IL)-1β,IL-6, IL-10,tumor necrosis factor α(TNF-α)and prostaglandin E2(PGE2)in serum and synovial membranes of all groups of rats were determined. RESULTS:Compared to the normal control group,the model control group demonstrated higher degree of primary and secondary toe swelling,arthritis index and levels of IL-1β,IL-6,TNF-αand PGE2 in serum and joint synovial membrane,and low-er level of IL-10 therein(P<0.01). Compared to the model control group,all the above-mentioned indexes of the rats in drug ad-ministration groups significantly improved(P<0.05 or P<0.01). CONCLUSIONS:The alcohol extract of T. asiatica. has a preven-tive and therapeutic effect on the model rats with AA by regulating the expression of anti-inflammatory and proinflammatory cyto-kines in serum and synovial membrane.

Objective To assess the effect of platycodin D(PD)for alleviating pulmonary fibrosis in mice and explore the underlying mechanism.Methods C57BL/6J mouse models of pulmonary fibrosis induced by bleomycin injection into the airway were treated with daily intragastric administration of 10 mg/kg PD for 28 days.The changes of pulmonary fibrosis and the expression and distribution of transient receptor potential cation channel subfamily C member 6(TRPC6)were evaluated with immunohistochemistry,HE staining and Sirius Red staining.Western blotting was used to detect α-SMA expression in the lung tissues of the mice.Primary cultures of mouse lung fibroblasts were pretreated with PD(2.5,5.0,and 10 μmol/L)or larixyl acetate(LA;10 μmol/L)before exposure to 10 ng/mL transforming growth factor-β1(TGF-β1),and the changes in cell survival rate,expressions of collagen I,α-SMA and TRPC6,reactive oxygen species(ROS)production,mitochondrial membrane potential,and cell proliferation capacity were assessed.Network pharmacology analysis was performed to explore the mechanism by which PD alleviated pulmonary fibrosis.Results PD treatment significantly alleviated pulmonary fibrosis and reduced α-SMA expression in BLM-induced mouse models(P<0.05).In TGF-β1-induced primary mouse lung fibroblasts,PD effectively inhibited the cell proliferation,reduced ROS production(P<0.0001),rescued the reduction of mitochondrial membrane potential(P<0.001),and inhibited the expressions of α-SMA and collagenⅠ(P<0.05).Network pharmacology analysis suggested that TRPC6 mediated the effect of PD for alleviating pulmonary fibrosis.Immunohistochemistry showed that PD significantly reduced TRPC6 expression in the lung tissues of BLM-induced mice.In primary mouse lung fibroblasts,PD significantly inhibited TGF-β1-induced TRPC6 expression(P<0.05),and LA treatment obviously lowered the expression levels of TRPC6,α-SMA and collagenⅠ(P<0.05).Conclusion PD alleviated pulmonary fibrosis in mice possibly by down-regulating TRPC6 and reducing ROS production.

Objective To assess the effect of platycodin D(PD)for alleviating pulmonary fibrosis in mice and explore the underlying mechanism.Methods C57BL/6J mouse models of pulmonary fibrosis induced by bleomycin injection into the airway were treated with daily intragastric administration of 10 mg/kg PD for 28 days.The changes of pulmonary fibrosis and the expression and distribution of transient receptor potential cation channel subfamily C member 6(TRPC6)were evaluated with immunohistochemistry,HE staining and Sirius Red staining.Western blotting was used to detect α-SMA expression in the lung tissues of the mice.Primary cultures of mouse lung fibroblasts were pretreated with PD(2.5,5.0,and 10 μmol/L)or larixyl acetate(LA;10 μmol/L)before exposure to 10 ng/mL transforming growth factor-β1(TGF-β1),and the changes in cell survival rate,expressions of collagen I,α-SMA and TRPC6,reactive oxygen species(ROS)production,mitochondrial membrane potential,and cell proliferation capacity were assessed.Network pharmacology analysis was performed to explore the mechanism by which PD alleviated pulmonary fibrosis.Results PD treatment significantly alleviated pulmonary fibrosis and reduced α-SMA expression in BLM-induced mouse models(P<0.05).In TGF-β1-induced primary mouse lung fibroblasts,PD effectively inhibited the cell proliferation,reduced ROS production(P<0.0001),rescued the reduction of mitochondrial membrane potential(P<0.001),and inhibited the expressions of α-SMA and collagenⅠ(P<0.05).Network pharmacology analysis suggested that TRPC6 mediated the effect of PD for alleviating pulmonary fibrosis.Immunohistochemistry showed that PD significantly reduced TRPC6 expression in the lung tissues of BLM-induced mice.In primary mouse lung fibroblasts,PD significantly inhibited TGF-β1-induced TRPC6 expression(P<0.05),and LA treatment obviously lowered the expression levels of TRPC6,α-SMA and collagenⅠ(P<0.05).Conclusion PD alleviated pulmonary fibrosis in mice possibly by down-regulating TRPC6 and reducing ROS production.

Objective:To investigate the effect of diabetes mellitus in the elderly on memory function in patients with mild cognitive impairment(MCI).Methods:Totally 449 community residents were selected for a 2-year follow-up survey.Montreal Cognitive Assessment(MoCA)and Mini-Mental State Examination(MMSE)were selected for overall cognitive function assessment.Fuld Object Memory(FOM)and Digital Span Test(DST)were used to evaluate delayed recall and instantaneous memory.Demographic data such as gender, age, education level, marital history, annual income, blood pressure, medical history etc.were collected.The glycosylated hemoglobin, fasting insulin, and carotid artery intima-media thickness were checked regularly.All subjects were grouped into non-diabetes mellitus normal cognitive group(NDM-NC group), non-diabetes mellitus mild cognitive impairment group(NDM-MCI group), diabetes mellitus normal cognitive group(DM-NC group)and diabetes mellitus mild cognitive impairment group(DM-MCI group).Results:In cross-sectional observation, the first, second, and last recall scores in the FOM showed a decreasing trend in the DM-MCI group, showed a word "U" -shaped fluctuation trend in the DM-NC group and the NDM-MCI group, and showed no significant change in the NDM-NC group.There were no significant differences in DST anterior-backward test scores between the DM-MCI group and NDM-MCI group(all P>0.05).Through longitudinal follow-up and two-by-two comparison with the other three groups, the average value of glycosylated hemoglobin in the DM-MCI group(6.78±0.60)% was the highest, and the differences were statistically significant( P<0.05).During follow-up, the average carotid intima-media thickness(CIMT)was higher in the DM-MCI group(1.03±0.20)mm than in NDM-NC group(0.89±0.20)mm( P<0.05), and the difference was statistically significant.Comparing with the other three longitudinal follow-up groups, the CIMT thickening speed in DM-MCI group was fastest. Conclusions:Elderly DM patient population have a higher prevalence of MCI, and their memory function fluctuates or declines significantly.Therefore, regular detection of memory function is conducive to delaying the progression of DM and MCI.

OBJECTIVE To investigate clinical efficacy and safety of Jipei dilong ointment combined with diacerein in the treatment of knee osteoarthritis （KOA） in the early and mid-term stage. METHODS Totally 100 KOA patients were randomly divided into control group and trial group， with 50 cases in each group. Control group received Diacerein capsules orally， 50 mg every time， bid. Trial group additionally received Jipei dilong ointment， once a day， on the basis of control group. Both groups had a treatment course of 4 weeks， and were followed up for 3 months after treatment. The clinical efficacy of 2 groups， visual analogue scale （VAS）， Western Ontario and McMaster University osteoarthritis index （WOMAC） score， Lysholm scores before and after treatment， at 3-month follow-up after treatment were all observed； the levels of tumor necrosis factor-α （TNF-α）， interleukin 1β （IL-1β）， IL-6， superoxide dismutase （SOD）， malondialdehyde （MDA）， nitric oxide （NO）， cartilage oligomeric matrix protein （COMP）， matrix metalloproteinase-13 （MMP-13） and C-telopeptide of type Ⅱ collagen （CTX-Ⅱ） were detected in knee joint fluid. The incidence of adverse drug reactions was recorded. RESULTS After 4 weeks of treatment， total effective rate was 96.0% in trial group and 90.0% in control group， without statistical significance between 2 groups （P＞0.05）. At 3- 2019YFC1712500） month follow-up after treatment， total effective rate of trial group was 94.0%， and was higher than 62.0% of control group（P＜0.05）. After 4 weeks of treatment and at 3-month follow-up after treatment， VAS score， WOMAC score，the contents ofTNF-α， IL-1β， IL-6， MDA， NO， COMP， MMP-13 and CTX-Ⅱ in knee joint fluid of two groups were significantly lower than before； Lysholm score and SOD activity of knee joint fluid were significantly higher than before， and the trial group was significantly better than the control group during the same period （P＜0.05）. And there was no statistical significance in the incidence of adverse drug reactions between two groups（P＞0.05）. CONCLUSION For the treatment of KOA in early and mid- term stage， Jipei dilong ointment combined with diacerein relieve pain， improve knee function by inhibiting inflammatory reaction， reducing oxidative stress and inhibiting chondrocyte and matrix degradation， and have low incidence of adverse drug reactions.

Animals ; Humans ; Thymic Stromal Lymphopoietin ; Pyroglyphidae/metabolism* ; Cytokines/metabolism* ; Asthma/metabolism* ; Respiratory System ; Epithelial Cells/metabolism*