tudca treatment  (MedChemExpress)

Journal: Laboratory investigation; a journal of technical methods and pathology

Article Title: Tauroursodeoxycholic acid inhibits experimental colitis by preventing early intestinal epithelial cell death.

doi: 10.1038/labinvest.2014.117

Figure Lengend Snippet: Figure 1 Disease activity parameters in TUDCA- and placebo-treated mice during DSS-induced colitis. (a) Mortality (censored data), (b) weight loss, (c) colon shortening, and (d–f) the expression of colonic proinflammatory cytokine IL1B protein levels, and Cxcl2 and Tnf mRNA expression during the course of DSS-induced colitis. NZ6 at each time point. *Po0.05, **Po0.01.

Article Snippet: DSS Induction and TUDCA Treatment Fifty-eight 8- to 10-week-old male C57BL/6 mice were purchased from Harlan (Harlan Laboratories, Horst, The Netherlands) and housed in a temperature-controlled room at 201C with a 12:12-h light-dark cycle.

Techniques: Activity Assay, Expressing

Journal: Laboratory investigation; a journal of technical methods and pathology

Article Title: Tauroursodeoxycholic acid inhibits experimental colitis by preventing early intestinal epithelial cell death.

doi: 10.1038/labinvest.2014.117

Figure Lengend Snippet: Figure 2 Histology and intestinal epithelial barrier function in TUDCA- and placebo-treated mice. (a) Histological scoring and representative images ( 200) of the colon of TUDCA- and placebo-treated mice at day 10 post DSS. (b) The number of bacteria found in the spleen at days 0 (no DSS), 7 and 14 post DSS and (c) quantitative analysis of periodic acid-Schiff staining in the colon of TUDCA- and placebo-treated animals during the course of DSS-induced colitis. (d) Representative images ( 1000) of periodic acid-Schiff-stained colon sections of TUDCA- and placebo-treated animals at days 0 (no DSS), 3, 10, and 14 post DSS. NZ6 at each time point. *Po0.05. NS, not significant; CFU, colony forming units.

Article Snippet: DSS Induction and TUDCA Treatment Fifty-eight 8- to 10-week-old male C57BL/6 mice were purchased from Harlan (Harlan Laboratories, Horst, The Netherlands) and housed in a temperature-controlled room at 201C with a 12:12-h light-dark cycle.

Techniques: Bacteria, Staining

Journal: Laboratory investigation; a journal of technical methods and pathology

Article Title: Tauroursodeoxycholic acid inhibits experimental colitis by preventing early intestinal epithelial cell death.

doi: 10.1038/labinvest.2014.117

Figure Lengend Snippet: Figure 3 Apoptotic markers in freshly isolated colonic epithelial cells following DSS administration in TUDCA- and placebo-treated mice. (a) Caspase-3 activity assessed using a DEVD-fluorogenic assay and (b) Bcl2 mRNA levels measured by qRT-PCR. NZ6 at each time point. *Po0.05, **Po0.01.

Article Snippet: DSS Induction and TUDCA Treatment Fifty-eight 8- to 10-week-old male C57BL/6 mice were purchased from Harlan (Harlan Laboratories, Horst, The Netherlands) and housed in a temperature-controlled room at 201C with a 12:12-h light-dark cycle.

Techniques: Isolation, Activity Assay, Quantitative RT-PCR

Journal: Laboratory investigation; a journal of technical methods and pathology

Article Title: Tauroursodeoxycholic acid inhibits experimental colitis by preventing early intestinal epithelial cell death.

doi: 10.1038/labinvest.2014.117

Figure Lengend Snippet: Figure 6 The effect of TUDCA on TNF-induced caspase-3 activation and apoptosis. (a) HT29 cells were stimulated with a combination of TNF and IFNG (TNF) for 24 h and treated with 1, 5, or 10 mM TUDCA, or an equal volume of medium. In the preincubation setting, TUDCA was added for 6 h, TUDCA was washed off and then the cells were stimulated with TNF for another 24 h. N ¼ 6 for each condition and the experiment was repeated four times. (b) Electron microscopic images ( 7000) of a monolayer of T84 cells stimulated with TNF with and without 10 mM TUDCA. Apoptotic bodies are indicated with arrows. **Po0.01 and ***Po0.001. RLU, relative light units.

Article Snippet: DSS Induction and TUDCA Treatment Fifty-eight 8- to 10-week-old male C57BL/6 mice were purchased from Harlan (Harlan Laboratories, Horst, The Netherlands) and housed in a temperature-controlled room at 201C with a 12:12-h light-dark cycle.

Techniques: Activation Assay

Journal: BMC molecular and cell biology

Article Title: RPL11 promotes non-small cell lung cancer cell proliferation by regulating endoplasmic reticulum stress and cell autophagy.

doi: 10.1186/s12860-023-00469-2

Figure Lengend Snippet: Fig. 4 Ribosomal protein L11 (RPL11) promotes non-small cell lung cancer (NSCLC) cell proliferation through endoplasmic reticulum stress (ERS) activa tion. (a,b) The effect of RPL11 on ERS-related protein expression levels in NSCLC cells were examined by western blotting. (c) The effect of ERS inhibitor (TUDCA) on ERS and atuophagy-related protein expression in RPL11-overexpressing NSCLC cells was detected by western blotting. The blots (a-c) were cut before hybridization with antibodies during blotting. The data are presented as mean ± SD from three independent trials (n = 3). Statistical data of a was analyzed using Student’s t-test, statistical data of b and c was analyzed using one-way ANOVA. *P < 0.05, **P < 0.01, ***P < 0.001

Article Snippet: Chloroquine (CQ) and tauroursodeoxycholic acid (TUDCA) treatment CQ (HY-17,589 A) and TUDCA (HY-19,696) were all purchased from MedChemExpress (Shanghai, China) and dissolved in DMSO.

Techniques: Expressing, Western Blot, Hybridization

Journal: Nutrition & Metabolism

Article Title: Oleic acid ameliorates palmitic acid induced hepatocellular lipotoxicity by inhibition of ER stress and pyroptosis

doi: 10.1186/s12986-020-0434-8

Figure Lengend Snippet: ER Stress induced NLRP3 inflammasome -mediated pyroptosis activation. The ER stress in HepG2 cells were elicited by chemical ER stressor tunicamycin (TM) for 24 h. a . Cell viability of cells was assessed using the CCK8 assay. b . and c . The mRNA expression of key genes governing ER stress and pyroptosis were detected after 24 h treatment of 0.8 uM TM, and β-ACTIN was used as an internal control. d . Representative western blots of ER stress and pyroptosis makers, and β-ACTIN was used as a protein-loading control. e . HepG2 cells were exposed to TM and plus with TUDCA or OA followed by labeling with anti-GSDMD or anti-NLRP3 antibody and were visualized under a microscope at 400× magnification after 24 h treatment. f . Cells were exposed to TM, or plus with TUDCA, 4-PBA or OA, and cell viability was assessed using the CCK8 assay. g . The mRNA expression of key genes governing ER stress and pyroptosis were detected after 24 h treatment, and β-ACTIN was used as an internal control. h . and i . Representative western blots of GRP78, CHOP, NLRP3 and GSDMD-N after 24 h treatment, and β-ACTIN was used as a protein-loading control. The data are presented as means ± SD for 3–5 biological replicates; * P < 0.05, ** P < 0.01, *** P < 0.001vs. BSA;# P < 0.05, ## P < 0.01,vs. TM; ns no significant differences between two connected groups

Article Snippet: When reaching about 80–90% confluence, cells were digested and cultured overnight in 96-well plates or 6-well plates.Then, the medium was changed to fresh medium containing 10% FBS, and different treatments.Tauroursodeoxycholic acid (TUDCA) and 4-phenylbutyrate (4-PBA) are chemical ER inhibitors, purchased from MedChemExpress (China).

Techniques: Activation Assay, CCK-8 Assay, Expressing, Control, Western Blot, Labeling, Microscopy

Journal: Nutrition & Metabolism

Article Title: Oleic acid ameliorates palmitic acid induced hepatocellular lipotoxicity by inhibition of ER stress and pyroptosis

doi: 10.1186/s12986-020-0434-8

Figure Lengend Snippet: Oleic acid abrogated pyroptosis in HepG2 cells through inhibiting ER stress. The ER stress in cells were inhibited by chemical chaperones 4-phenylbutyric acid (4-PBA) or tauroursodeoxycholic acid (TUDCA) for 24 h against ER stress. a . and b . Cell viability of HepG2 cells was assessed using CCK8 assay. c . The mRNA expression of key genes governing pyroptosis were detected after 24 h treatment, and β-ACTIN was used as an internal control. d . Representative western blots of NLRP3 and GSDMD-N after 24 h treatment, and β-ACTIN was used as a protein-loading control. e . HepG2 cells were exposed to PA or plus OA, TUDCA or 4-PBA followed by labeling with anti-GSDMD (red) antibody and DAPI staining, and were visualized under a microscope at 100× magnification after 24 h treatment. f . and g . Cell supernatants were analyzed for IL-1β and TNF-α secretion by HepG2 cells by ELISA. The data are presented as means ± SD for 3–5 biological replicates; * P < 0.05, ** P < 0.01, and *** P < 0.001vs. BSA;# P < 0.05, ## P < 0.01vs.PA ;ns no significant differences between two connected groups

Article Snippet: When reaching about 80–90% confluence, cells were digested and cultured overnight in 96-well plates or 6-well plates.Then, the medium was changed to fresh medium containing 10% FBS, and different treatments.Tauroursodeoxycholic acid (TUDCA) and 4-phenylbutyrate (4-PBA) are chemical ER inhibitors, purchased from MedChemExpress (China).

Techniques: CCK-8 Assay, Expressing, Control, Western Blot, Labeling, Staining, Microscopy, Enzyme-linked Immunosorbent Assay