ObjectiveTo investigate the relationship between the nucleotide binding oligomerization domain like receptor protein 3 (NLRP3) inflammasome and inflammatory reaction of venous ulcer of lower extremity.MethodsTwenty-four patients with active venous ulcer of lower extremity (active ulcer group), 24 patients with non exudative venous ulcer of lower extremity as positive control (non-active ulcer group), and 24 patients with traumatic wound as negative control (traumatic-wound group) were enrolled. The clinical data of the three groups were compared, the tissue samples around the wound were harvested, and the expressions of NLRP3 protein were detected by immunohistochemistry among the three groups. Enzyme linked immunosorbent assay (ELISA) was used to detect the IL-1β and IL-18 protein levels, RT-PCR was used to detect the mRNA expressions of apoptosis associated speck like protein containing CARD (ASC), caspase-1, c-Jun N-terminal kinase (JNK), p38, nuclear factor (NF)-κB p65 and NF-κB inhibitor alpha (NF-κB IkBα), and Western blotting was performed to evaluate the level of NLRP3 inflammasome in wound tissues.ResultsThe inflammatory response in the non-active ulcer group and trauma-wound group were milder than that in the active ulcer group. The levels of IL-1β and IL-18 proteins in the active ulcer group were higher than those in the non-active ulcer group and the traumatic-wound group [IL-1β: (146.621±11.597) ng/L vs. (80.967±14.213) ng/L vs. (84.962±19.484) ng/L, F=136.200, P<0.001; IL-18: (119.814±12.788) ng/L vs. (72.899±17.220) ng/L vs. (48.131±10.407) ng/L, F=167.910, P<0.001]. The results of RT-PCR showed that the mRNA expressions of ASC [(0.030±0.012) ng/L vs. (0.021±0.005) ng/L vs. (0.016±0.004) ng/L, F=18.106, P<0.001], caspase-1 [(0.054±0.012) ng/L vs. (0.013±0.009) ng/L vs. (0.018±0.006) ng/L, F=130.372, P<0.001], NF-κB p65 [(0.093±0.015) ng/L vs. (0.038±0.013) ng/L vs. (0.043±0.014) ng/L, F=110.950, P<0.001], NF-κB IkB-α [(0.085±0.015) ng/L vs. (0.078±0.015) ng/L vs. (0.041±0.016) ng/L, F=53.070, P<0.001], and JNK [(0.075±0.018) ng/L vs. (0.042±0.013) ng/L vs. (0.039±0.014) ng/L, F=41.271, P<0.001] in the wound tissues of the active ulcer group were higher than those in the non-active ulcer group and the traumatic-wound group. And the mRNA expression of p38 in the wound tissues of the active ulcer group was lower than that in the non-active ulcer group [(0.050±0.008) ng/L vs. (0.064±0.014) ng/L, P<0.05]. The result of Western blotting showed that the relative expression level of NLRP3 protein in the wound tissues of the active ulcer group was higher than that in the trauma-wound group and non-active ulcer group (0.767±0.272 vs. 0.605±0.212 vs. 0.556±0.183, F=4.804, P=0.012).ConclusionNLRP3 inflammasome is closely related to the wound in venous ulcer of lower extremity and provides a new target to the therapy of venous ulcer of lower extremity.
ObjectiveTo observe the efficacy and safety of etofenamate gel (foscavir+tramadoli hydrochloridum+gabapentin) in the treatment of acute herpes zoster. MethodsForty patients with acute herpes zoster neuralgia treated between January 2013 and June 2014 were randomly divided into two groups:control group and treatment group, with 20 in each. The patients had a visual analogue scale (VAS) pain score of seven or higher. Patients in the control group accepted conventional treatment, while those in the treatment group were treated with conventional treatment combined with etofenamate gel. Two weeks after treatment, VAS score, quality of life and sleep score, and the degree of improvement in skin paresthesia were evaluated and compared between the two groups. ResultsThe VAS score decreased significantly in both the two groups after treatment (P < 0.05), and the decrease in the treatment group was significantly more obvious (P < 0.05). The quality of life, sleep score and the degree of improvement in skin paresthesia were ameliorated significantly after treatment (P < 0.05), and the amelioration in the treatment group was significantly greater (P < 0.05). ConclusionThe early application of Ordofen can strengthen analgesia effect of the conventional treatment, improve the quality of life and sleep, and reduce skin paresthesia.
Objective To investigate the role of inflammatory factors like serumleptin, adiponectin,interleukin-6( IL-6) , and C-reactive protein ( CRP) in the systemic inflammatory response of smokinginduced COPD. Methods Thirty male Wistar rats were randomly divided into three groups, ie. a high-dose smoking group, a low-dose smoking group, and a control group. Serum leptin, adiponectin, IL-6, and CRP levels were measured by ABC-ELISA. Results The serum leptin and adiponectin levels in both smoking groups decreased significantly compared with the control group( P lt; 0. 05) , while the difference was not significant between the two smoking groups ( P gt; 0. 05) . The serum IL-6 and CRP levels in both smoking groups increased significantly compared with the control group( P lt; 0. 05) , which were higher in the highdosesmoking group than those in the low-dose smoking group( P lt;0. 05) . Conclusions Smoking increases the serum levels of IL-6 and CRP, but reduces the serum levels of leptin and adiponectin in rats. These results suggest that leptin, adiponectin, IL-6, and CRP may be involved in the systemic inflammatory response of smoking-induced COPD.
Objective To assess the efficacy of topical non-steroidal anti-inflammatory drugs （NSAIDs） in the treatment of osteoarthritis （OA）. Methods MEDLINE, EMBASE, Scientific Citation Index, CINAHL, The Cochrane Library, CBMdisc and abstracts from conference were searched from 1966 to March 30, 2005. Randomized controlled trials （R.CT） comparing topical non-steroidal anti-inflammatory drug （NSAIDs） with placebo or oral NSAIDs in OA were induded. Effect size （ES） was calculated for pain, function and stiffness. Relative risk （RR） was calculated for dichotomous data such as clinical response rate and adverse effect rate. Number needed to treat to obtain the clinical response was estimated. The quality of trials was assessed and sensitivity analyses were undertaken. Results Topical NSAIDs were superior to placebo in relieving pain due to osteoarthritis only in the first 2 weeks of treatment; ES （95% CI） were 0.41 （0. 16 to 0.66） and 0.40 （0.15 to 0.65） at week 1 and 2 respectively. However, the effects were short-lived and no benefit was observed over placebo at the third and fourth week. A similar pattern was observed with function, stiflhess and clinical response RR and number needed to treat. Topical NSAIDs were inferior to oral NSAIDs at week 1, and associated with more local side effects such as rash, itch or burning （RR 5.29, 95% CI 1.14 to 24. 51 ）. Conclusions Only very shortterm （less than 4 weeks） RCTs have assessed topical NSAID efficacy in OA ; after 2 weeks no efficacy above placebo has been obsevrved. There are no trial data to support the long-term use of topical NSAIDs in osteoarthritis.
ObjectiveTo elucidate the characteristics of colonic Crohn’s disease (CD) and evaluate effectiveness of surgical treatment.MethodClinical data of 28 cases with colonic CD who underwent surgery at West China Hospital of Sichuan University between Feb. 2009 and Jan. 2017 were retrospectively analyzed.ResultsDefinite diagnosis of colonic CD was performed in 12 cases preoperatively (42.9%), but 16 cases (57.1%) were misdiagnosed as other disease, ulcerative colitis (5 cases, 17.9%), tumor (4 cases, 14.3%), appendiceal disease (4 cases, 14.3%), and intestinal tuberculosis (3 cases, 10.7%) were the major causes of preoperative misdiagnosed disease. Of the 28 cases, elective surgery was performed in 26 cases and emergency surgery in 2 cases. The major surgical procedures were segmental colectomy(10 cases) and right hemicolectomy (6 cases), as well as ilecolostomy (9 cases), colocolostomy(6 cases), ileostomy(9 cases), colostomy (6 cases), and so on. The length of the first hospital stay of operation related to intestinal lesions in this group was 5–74 d (mean of 25.4 d). Postoperative complications were occurred in 9 cases (32.1%), all these cases didn’t receave medical treatment. Twenty cases were followed up, and the follow-up time was 7–78 months (mean of 33.4 months), 8 cases lost follow-up. The prognosis of the follow-up cases was good.ConclusionsColonic CD has occult clinical manifestation, resulting in misdiagnosis and mistreatment. Segmental resection of the colon is the important treatment for colonic CD. For patients with complications, multidisciplinary diagnosis and treatment is necessary. In addition, systematic medical treatment before surgery helps to reduce the risk of the first surgery associated with intestinal lesions.
Objective To determine the relationship between preoperative prognostic inflammatory and nutritional index (PINI) value and short-term prognosis in colorectal cancer. Methods Patients with colorectal cancer verified by pathologically examine were prospectively enrolled from April 2009 to June 2009. Serum alpha-1-acid glycoprotein, C-reactive protein, albumin and prealbumin were examined on day 3 before operation, and the value of preoperative PINI was calculated. The relationships between preoperative PINI and patho-TNM stage, complications, quality of life, and recurrence and metastasis after operation were analyzed. Results Total 38 patients with colorectal cancer underwent radical surgery were enrolled. Preoperative PINI value was 2.17±1.27. Preoperative PINI value was correlated with TMN stage and M stage: PINI value in patients of Ⅳ stage or M1 stage, were significantly higher than those in ones of Ⅰ, Ⅱ and Ⅲ stage （P＜0.001） or M0 stage （P＜0.001）. There was no significant correlation between preoperative PINI value and preoperative complications （Pgt;0.05）. Preoperative PINI value was correlated with postoperative diet, anorexia and overall quality of life: preoperative PINI value in patients with abnormal diet, anorexia or poor quality of life, were significantly higher than those in ones with normal diet (P=0.020), no-anorexia (P=0.020) or moderate (P=0.025) and well (P=0.020) quality of life. Conclusion Preoperative PINI value is an effective index to assess the short-term prognosis of colorectal cancer.
ObjectiveTo investigate the influence of endoplasmic reticulum stress (ERS) on smoking-induced nucleus pulposus cells apoptosis and inflammatory response.MethodsBetween October 2016 and October 2018, 25 patients with cervical disc herniation receiving discectomy were collected and divided into smoking group (14 cases) and non-smoking group (11 cases). The baseline data of age, gender, herniated segment, and Pfirrmann grading showed no significant difference between the two groups (P>0.05). The obtained nucelus pulposus tissues were harvested to observe the cell apoptosis via detecting the apoptosis-related proteins (Caspase-3 and PRAP) by TUNEL staining and Western blot test. The nucleus pulposus cells were isolated and cultured with enzyme digestion, of which the third generation cells were used in follow-up experiments. Then, the expressions of inflammatory factors [interleukin 1β (IL-1β) and tumor necrosis factor α (TNF-α)] were detected by ELISA; the nuclear translocation of P65 was monitored by cell immunofluorescence staining. Furthermore, ERS-related proteins (GRP78 and CHOP) were detected by Western blot; and endoplasmic reticulum ultrastructure was observed under transmission electron microscope. To verify the regulatory effect of ERS, cells were pretreated by ERS specific inhibitor (4-PBA), then cell apoptosis and inflammatory response were tested.ResultsThe nucleus pulposus tissue observation showed that the cell apoptotic rate and the expressions of apoptosis-related proteins (Caspase-3 and PARP) were obviously higher in smoking group than in non-smoking group (P<0.05). The nucleus pulposus cells observation indicated that the expressions of the inflammatory factors (IL-1β and TNF-α) and the ERS-related proteins (GRP78 and CHOP) were also higher in smoking group than in non-smoking group (P<0.05). The results of cell immunofluorescence staining further confirmed that smoking stimulated nuclear translocation of P65 in nucleus pulposus cells. The ERS injury was much more serious in smoking group than in non-smoking group. Furthermore, after 4-PBA inhibiting ERS, the expressions of GRP78, CHOP, IL-1β, TNF-α, and P65 were significantly decreased (P<0.05), and flow cytometry results showed that cell apoptotic rate in smoking group was decreased, showing significant difference compared with the non-smoking group (P<0.05).ConclusionSomking can stimulate cell apoptosis and inflammatory response in nucleus pulposus cells via ESR pathway. Suppressing ESR may be a novel target to suspend smoking-induced intervertebral disc degeneration.
Radiofrequency ablation for hepatic hemangioma is safe and effective, and can obtain the same curative effect as traditional surgical resection. For hepatic hemangiomas with large volume, abundant arterial blood supply and long ablation time, systemic inflammatory response syndrome (SIRS) often occurs after radiofrequency ablation, which can lead to injury or dysfunction of important organs. This paper systematically summarizes the mechanism, prevention and treatment of SIRS after radiofrequency ablation of hepatic hemangioma, so as to provide reference for improving the safety of radiofrequency ablation of hepatic hemangioma.
Objective To develop a diclofenac sodium-loaded gelatin scaffold with anti-inflammatory activity and provide a new avenue for alleviating the inflammatory response and enhancing cartilage regeneration in vivo. Methods Diclofenac sodium was homogeneously mixed with gelatin to prepare a diclofenac sodium-loaded porous gelatin scaffold by freeze-drying method as the experimental group, and a pristine porous gelatin scaffold was served as a control group. The general morphology of the scaffold was observed, the pore size of the scaffold was measured by scanning electron microscopy, the porosity of the scaffold was calculated by drainage method, the loading of diclofenac sodium into the gelatin scaffold was detected by fourier transform infrared spectrometer and X-ray diffraction examinations, and the release kinetics of diclofenac sodium from gelatin scaffold was tested using an in vitro release assay. The two scaffolds were co-cultured with lipopolysaccharide-predisposed RAW264.7 in vitro, and the expressions of interleukin 1β (IL-1β) and tumor necrosis factor α (TNF-α) were detected by reverse transcription polymerase chain reaction (RT-PCR), enzyme-linked immuno sorbent assay, and Western blot, to detect the in vitro anti-inflammatory effect of the drug-loaded scaffold. Thereafter, the second generation chondrocytes of New Zealand white rabbits were inoculated on the two groups of scaffolds for in vitro culture, and the cytocompatibility of the scaffold was tested by live/dead staining and cell counting kit 8 assay, the feasibility of in vitro cartilage regeneration of the scaffold was evaluated via gross observation, HE staining, Safranin-O staining, and immunohistochemical collagen type Ⅱ staining, as well as biochemical quantitative analyses. Finally, the two groups of chondrocyte-scaffolds were implanted subcutaneously into New Zealand white rabbits, and after 4 weeks, the general observation, HE staining, safranin O staining, immunohistochemical collagen type Ⅱ staining, and biochemical quantitative analyses were performed to verify the cartilage regeneration in vivo, and the expression of inflammation-related genes CD3 and CD68 was detected by RT-PCR to comprehensively evaluate the anti-inflammatory performance of the scaffolds in vivo. Results The two scaffolds exhibited similar gross, microporous structure, pore size, and porosity, showing no significant difference (P>0.05). Diclofenac sodium was successfully loaded into gelatin scaffold. Data from in vitro anti-inflammatory assay suggested that diclofenac sodium-loaded gelatin scaffold showed alleviated gene and protein expressions of IL-1β and TNF-α when compared with gelatin scaffold (P<0.05). The evaluation of cartilage regeneration in vitro showed that the number of living cells increased significantly with the extension of culture time, and there was no significant difference between the two groups at each time point (P>0.05). White cartilage-like tissue was regenerated from the scaffolds in both groups, histological observation showed typical cartilage lacuna structure and specific cartilage extracellular matrix secretion. There was no significant difference in the content of cartilage-specific glycosaminoglycan (GAG) and collagen type Ⅱ between the two groups (P>0.05). In vivo experiments showed that the samples in the experimental group had porcelain white cartilage like morphology, histologic staining showed obvious cartilage lacuna structure and cartilage specific extracellular matrix, the contents of GAG and collagen type Ⅱ were significantly higher than those in the control group, and the protein and mRNA expressions of CD3 and CD68 were significantly lower than those in the control group, with significant differences (P<0.05). ConclusionThe diclofenac sodium-loaded gelatin scaffold presents suitable pore size, porosity, and cytocompatibility, as well as exhibited satisfactory anti-inflammatory ability, providing a reliable scheme for alleviating the inflammatory reaction of regenerated cartilage tissue after in vivo implantation and promoting cartilage regeneration in vivo.
Objective To introduce the inflammatory microenvironment and epithelial-mesenchymal transition process of hepatocellular carcinoma, and review the relationship between them. Methods Domestic and international literatures were collected to summary the relationship between epithelial-mesenchymal transition and the inflammatory microenvironment of hepatocellular carcinoma. Result Many inflammatory factors and viral gene encoding proteins in the inflammatory microenvironment play an important role in the process of epithelial-mesenchymal transition in hepatocellular carcinoma. Conclusions The inflammatory microenvironment of hepatocellular carcinoma is an indispensable role in the process of epithelial-mesenchymal transition. The inhibition and treatment of inflammatory microenvironment may play a more active role in the control of tumor invasion and metastasis.