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Aim To investigate the effect of p-hydroxybenzaldehyde ( HD) on intestinal fibrosis in mice based on mouse intestinal fibrosis model and in vitro EMT model,and to explore the underlying mechanism Methods HE staining, Masson staining, immunohisto-chemistry ,qPCR, Western blot and other experimental methods were used to verify the effect of HD on intestinal fibrosis in mice and the potential mechanism. Results In vivo experiments showed that compared with the normal group, the DSS-induced intestinal fibrosis model group had shortened colon, increased colon his-topathological score, increased collagen volume fraction, and significantly increased collagen I expression. After treatment with 4, 10, and 25 mg • kg
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Objective To provide the basis for endoscopic craniocervical junction surgery through cervical CT image and endoscopic odontoid process anatomy of atlas, axis and odontoid. Methods A total of 150 cases of cervical vertebrae were selected for high resolution thin slice plain CT measurement to evaluate the atlantoaxial structure and its adjacent structure, and to estimate the safe boundary of odontoid process resection. The atlantoaxial odontoid process was anatomized on 3 cadaver head specimens under endoscope through the submandibular approach using STORZ endoscopy system and endoscopic surgical instruments. Results The average length of atlas anterior arch and other anatomical marks were measured by CT, and the safety boundary area of odontoidectomy was estimated to be（240.9 ± 39.92）mm~2, male:（248.3 ± 49.64）mm~2, Female:（233.2 ± 24.54）mm~2. Through the submandibular endoscopic approach, the atlantoaxial anatomy and odontoidectomy anatomy made a transverse incision at the midpoint of the connecting line between one mandibular angle and hyoid bone to expose the submandibular triangle area. Under the endoscope, the digastric muscle and the greater angle of hyoid bone were exposed through the submandibular triangle area, and the retropharyngeal space was passively separated layer by layer to the prevertebral space to expose the prevertebral fascia. After removing the prevertebral tissue, the atlas, the dentate process of the axis, the atlantooccipital joint, the atlantoaxial joint, and part of the foramen magnum were fully exposed. Conclusion Estimating odontoid resection safety boundary area by CT image, in combination with endoscopic odontoidectomy anatomy via sunbmandibular approach, we can perform the surgery safely and efficiently under the bright of endoscope with surgical instruments, which can significantly reduce the incidence of cerebrospinal fluid leakage and postoperative infection while decompressing.
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Objective To investigate the intestinal mucosal barrier function protective effect of ulinastatin in sepsis rats and its effect on Wnt/β-catenin signaling pathway. Methods One hundred SD rats were randomly divided into control group, sepsis group, ulinastatin group, XAV939+ulinastatin group and lithium chloride( LiCl) +ulinastatin group. The classical cecal ligation was used to duplicate sepsis model, and the jejunal mucosal injury was evaluated. The levels of inflammatory factors interleukin (IL)-6 and tumor necrosis factor(TNF)-α were detected by ELISA, and the expressions of β-catenin and cyclin D1 were detected by Real-time PCR and Western blotting. We also observed the effect of the Wnt signal pathway blockage by XAV939 or Wnt signal pathway activator by LiCl on ulinastatin protection of intestinal mucosa and proteins related to the Wnt signal pathway. Results The levels of IL-6, TNF-α and intestinal mucosal injury in the sepsis group were significantly higher than those in the ulinastatin group. The mRNA and protein expression levels of β- catenin and cyclin D1 in the sepsis group were significantly higher than those in the control group (P<0.05), After ulinastatin treatment, the expression levels of β-catenin and cyclin D1 mRNA and protein were significantly decreased, and the difference was significant (P<0.05). Compared with the ulinastatin group, combined treatment with XAV939 promoted the protective effect of ulinastatin on the intestinal mucosa of rats, and the protein expression of β-catenin and cyclin D1 was reduced (P<0.05). Combined treatment with LiCl weakened the protective effect of ulinastatin on the intestinal mucosa of rats, and the protein expression of β-catenin and cyclin D1 was increased (P<0.05). Conclusion Ulinastatin may inhibit the Wnt signaling pathway by down-regulating the expression of β-catenin, reduce the expression of inflammatory factors IL-6 and TNF-α, thereby promote repairing the intestinal mucosal barrier function damage.
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We cloned flavonol synthase gene (named as CmFLS) by RACE from Chrysanthemum morifolium cv. 'Hangju' based on transcriptome database. Sequencing results showed that 1 235 bp sequence was acquired with the largest open reading frame (ORF) of 1 008 bp, which encoded 335 amino acids. The predicted CmFLS encoded protein had an isoelectric point (pI) of 5.41. The phylogenetic tree analysis indicated that CmFLS was highly homologous to other FLSs, which identified from the species of Compositae. The recombinant fusion protein, with a molecular mass of 43 kDa, was successfully expressed by prokaryotic expression system. Meanwhile, Ni-NTA resin was used to purify the recombinant fusion protein, and the Ni-Native Buffer containing 250 mmol·L⁻¹ imidazole was most favorable for elution. The purified recombinant fusion protein was subjected to in vitro catalytic reaction, and then the products were extracted and analyzed by HPLC. The results showed that the recombinant fusion protein CmFLS was able to catalyze the production of quercetin by dihydroquercetin under specific buffer and reaction conditions, which indicated that the functional protein encoded by CmFLS had dioxygenase activity in the biosynthetic pathway of flavonoids biosynthesis in Ch. morifolium cv. 'Hangju'. The above results laid the foundation for further studying on CmFLS, and provided new ideas for the regulation of flavonoids metabolism from the molecular level and the catalytic synthesis of flavonols in vitro.
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Aim To investigate the role of P2X7 recep-tor and its mediated NLRP3 inflammatory signaling pathway in alcohol-induced liver injury. Methods The acute alcoholic liver injury model was established by NIAAA method, and thirty C57BL/6 male mice were randomly divided into three groups (n =10):control group, model group, A438079 group, The three groups were processed as follows in the last week:control group and model group: given an equal dose of saline intraperitoneal injection(about 0.2 mL/only) once a day. According to the weight of the mice, A438079 group was given intraperitoneally injection by 200 μmol·kg-1of A-438079 (prepared at 7 g·L-1 of A438079,about 0.2 mL/only) once a day. And it was given a single 31.5% alcohol solution by intragas-tric administration on the last day of the morning,with the dose of 10 mL·kg-1. Nine hours later alanine aminotransferase (ALT), aspartate aminotransferase (AST),cholesterol(TCHO),triglyceride(TG) were measured by orbital blood in mice. HE staining was used to observe the pathological changes of the liver. Immunohistochemical method was applied to detect the expression of P2X7R in liver tissues. Western blot was employed to detect the levels of P2X7R, NLRP3, ASC, IL-1β and IL-18 in liver tissues. Results Compared with control group,the levels of ALT,AST, TG and TCHO in model group were significantly en-hanced, and the liver injury was obvious. Compared with model group, the levels of ALT, AST, TG and TCHO in A438079 group significantly decreased. Compared with control group, the expressions of P2X7, NLRP3, ASC, IL-1β, IL-18 in model group were significantly higher than those in control group. Compared with model group, the expression levels of P2X7, NLRP3, ASC, IL-1β and IL-18 in A438079 group significantly decreased. Conclusion Alcohol-induced liver injury may be associated with P2X7R-NLRP3 signaling pathway.
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OBJECTIVE@#To compare the nephrotoxicity of high- and low-osmolar contrast media (HOCM and LOCM), and to determine the protective role of fosinopril or telmisartan and its possible mechanism.@*METHODS@#Forty eight healthy SD rats were randomly divided into 6 groups: a normal control group, a glycerol control group, a low-osmolar contrast media (LOCM) group, a high-osmolar contrast media (HOCM) group, a fosinopril group, and a telmisartan group. Glycerine for inducing kidney damage was given to all rats except the normal control group. Twenty-four hours after the injection of glycerine, the mixed fosinopril suspension (10mg/kg) or telmisartan (5mg/kg) was poured into the stomach in the preventive group. Serum creatinine (SCr) and plasma angiotensin II (AngII) levels were detected by an automatical biochemical analyzer and radioimmunoassay; caspase-3 activity and claudin-1 expression of the renal tissue were detected by fluorometric method and immunohistochemical method. The renal injury was assessed by hematoxylin and eosin (HE) staining and terminal deoxynucleotide mediated nick and labeling (TUNEL) staining, respectively.@*RESULTS@#In diatrizoate-injected rats, SCr and AngII levels were increased (P<0.05). Expression of claudin-1 protein and caspase-3 activity in the renal tissue was upregulated. The histologic changes and percentage of apoptotic cells were milder in the LOCM rats than those in the HOCM rats. In the group pretreated with fosinopril or telmisartan, no increase in the levels of SCr and AngII was discovered. The expression of claudin-1 protein and caspase-3 activity was significantly lower than that in the HOCM group. The renal injuries induced by diatrizoate were alleviated.@*CONCLUSION@#Both HOCM and LOCM could cause cellular apoptosis in the kidney.LOCM was less toxic to rat kidney than HOCM. Nephrotoxicity induced by HOCM might be related to caspase-3, claudin-1 and AngII. Fosinopril or telmisartan may protect the renal tissue from nephrotoxicity induced by diatrizoate.