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BACKGROUND:Kidney deficiency and blood stasis syndrome are common traditional Chinese medicine syndromes observed in knee osteoarthritis,which serve as fundamental pathogenesis factors.There exists a significant connection between the two.Previous studies have demonstrated that kidney deficiency and blood stasis syndrome effectively contribute to knee joint cartilage degeneration and the progression of knee osteoarthritis.However,the mechanisms underlying the promotion of knee joint cartilage damage remain unclear and require further investigation. OBJECTIVE:To investigate the influence of kidney deficiency and blood stasis syndrome on the progression of knee osteoarthritis in Sprague-Dawley rats. METHODS:Sixteen Sprague-Dawley rats were randomly divided into two groups:a model observation group and a control group,with eight rats in each group.Animal models of kidney deficiency were induced by ovary removal in the model observation group,while the control group was given a sham procedure for ovarian removal.Two months after modeling,both groups underwent modified HULTH surgery to induce knee osteoarthritis.One week after modified HULTH surgery,the model observation group was subcutaneously given adrenaline hydrochloride to make blood stasis models,while the control group was subcutaneously given normal saline.At the 5th week after modified HULTH surgery,blood rheology,coagulation parameters,triiodothyronine,tetraiodothyronine,and estradiol levels were measured.Knee joint X-ray images were taken,and knee joint sections were stained with safranin O-fast green,hematoxylin-eosin,and immunohistochemistry. RESULTS AND CONCLUSION:Compared with the control group,the model observation group exhibited significant increases in whole blood viscosity at low,medium,and high shear rates,as well as increased plasma viscosity.Fibronectin levels in the coagulation parameters were significantly increased,while prothrombin time and activated partial thromboplastin time were significantly decreased.Triiodothyronine,tetraiodothyronine,and estradiol levels were all significantly decreased.Radiographic results showed that the model observation group exhibited more severe degree of knee joint space narrowing and surface roughness,with the appearance of high-density shadows.Hematoxylin-eosin and safranin O-fast green staining demonstrated more severe cartilage damage in the model observation group,with significantly higher OARSI and Mankin scores compared with the control group.Compared with the control group,immunohistochemistry results showed a significant reduction in the expression of extracellular matrix type II collagen and aggrecan protein in the cartilage of the model observation group rats.Moreover,there was a significant increase in the expression of matrix metalloproteinase 13 and aggrecanase 5,which are inflammatory factors.These results indicate that the Sprague-Dawley rat model of knee osteoarthritis with kidney deficiency and blood stasis was successfully established.Kidney deficiency and blood stasis syndrome further aggravate cartilage extracellular matrix degradation and cartilage degeneration by promoting the expression of inflammatory factors,thereby promoting the progression of knee osteoarthritis in rats.
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To analyze the correlation between lipid profile and disease activity in patients with inflammatory bowel disease (IBD).A total of 307 Crohn′s disease (CD) patients, 232 ulcerative colitis (UC) patients and 165 healthy subjects from the same geographic region were included. Total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C) and lipoprotein(a)[Lp(a)] were retrieved from their medical records. Crohn disease activity index (CDAI) and Mayo scores were calculated as measurement of disease severity for CD and UC separately. Patients with CD and UC had lower TC, TG, HDL-C and LDL-C levels than those in control group ( P<0.05). Additionally, CDAI was negatively associated with TC, HDL-C and LDL-C levels ( r=-0.218, -0.210, -0.176, P<0.05), while TG level was not associated with CDAI. Mayo scores was not significantly associated with TC, HDL-C, LDL-C and TG. Patients with CD had higher Lp(a) levels than those in UC and control group ( P<0.05). Furthermore, patients with active CD had higher Lp (a) levels than those with inactive disease ( P<0.05).The Lp(a) levels in CD patients were positively associated with CDAI ( r=0.151, P<0.05), while Lp(a) level in UC group was nor assocriated with Mayo score. Patients with IBD have dyslipidemia and lipid profile is associated with disease activity in CD patients.
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Objective:Mesenteric fat hypertrophy is present in about a quarter of Crohn′s disease (CD) patients and it can be easily detected by bowel ultrasound (US). The purpose of this research was to assess the correlation between mesenteric fat hypertrophy and behavior and activity of CD.Methods:A total of 89 CD patients who admitted to the First Affiliated Hospital of Nanjing Medical University from August 2018 to November 2019 were recruited in this study. The total CD patients were divided into two groups depending on with or without mesenteric fat hypertrophy by US tests. Crohn′s disease activity index (CDAI), simplified endoscopic score for Crohn′s disease (SES-CD), serum inflammatory indicators and fecal calprotectin were assessed.Results:Mesenteric fat hypertrophy was significantly associated with stricturing behavior (B2, P<0.01). CDAI ( P=0.002) , blood platelet ( P=0.001) , C-reactive protein ( P=0.024) , fecal calprotectin ( P=0.004) and bowel wall thickness ( P<0.01) in patients with mesenteric fat hypertrophy were significantly higher than those without, but not the erythrocyte sedimentation rate ( P=0.110) and SES-CD ( P=0.115) . Serum albumin ( P=0.001) in patients with mesenteric fat hypertrophy was lower than that in patients without mesenteric fat hypertrophy. Conclusion:Mesenteric fat hypertrophy is correlated with intestinal stenosis and disease activity in patients with Crohn′s disease.
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@#Thirteen compounds were isolated and purified from the ethanol extract of Clerodendrum trichotomum Thunb. by various chromatographic methods. Their structures were identified as friedelin(1), betulinic acid(2), taraxerol(3), platanic acid(4), acacetin(5), 5, 7-dihydroxy 3′, 4′-dimethoxyflavone(6), β-sitosterol(7), stigmasterol(8), daucosterol(9), stigmasterol-3-O-glucopyranoside(10), isovanillin(11), dibutyl phthalate(12)and syringaldehyde(13). Compounds 4, 6, 11- 13 were isolated from genus Clerodendrum Linn. for the first time. Compounds 4, 6, 10- 13 were isolated from Clerodendrum trichotomum Thunb. for the first time.
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OBJECTIVE:To investigate the effect of edelfosine on the proliferation of Hela cells and its mechanism.METHODS:Hela cells were treated with edelfosine at doses of 0(control),0.5,1.0,5.0,10.0 ?mol?L-1 for 96 h.MTT assay,flow cytometry,and staining were performed to determine the cell proliferation activity,cell cycle,and apoptotic rate.RESULTS:As compared with control,the cell proliferation activity of Hela cells was inhibited in a dose-and time-dependent manner after being treated by edelfosine for 24～96 h.After being treated by edelfosine(1.0,5.0,10.0 ?mol?L-1) for 72 h,the number of Hela cells significantly increased in G0/G1 phase but decreased in S phase(P