scholarly journals Melatonin modulates microsomal PGE synthase 1 and NF-E2-related factor-2-regulated antioxidant enzyme expression in LPS-induced murine peritoneal macrophages

2013 ◽  
Vol 171 (1) ◽  
pp. 134-144 ◽  
Author(s):  
M Aparicio-Soto ◽  
C Alarcón-de-la-Lastra ◽  
A Cárdeno ◽  
S Sánchez-Fidalgo ◽  
M Sanchez-Hidalgo
Keyword(s):  
Antioxidant Enzyme ◽  
Peritoneal Macrophages ◽  
Related Factor ◽  
Enzyme Expression ◽  
Murine Peritoneal Macrophages

scholarly journals Terminalia bellirica (Gaertn.) Roxb. Extract and Gallic Acid Attenuate LPS-Induced Inflammation and Oxidative Stress via MAPK/NF-κB and Akt/AMPK/Nrf2 Pathways

2018 ◽  
Vol 2018 ◽  
pp. 1-15 ◽  
Author(s):  
Miori Tanaka ◽  
Yoshimi Kishimoto ◽  
Mizuho Sasaki ◽  
Akari Sato ◽  
Tomoyasu Kamiya ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protein Kinase ◽  
Gallic Acid ◽  
Antioxidant Enzyme ◽  
Related Factor ◽  
Nuclear Factor ◽  
Ros Production ◽  
Enzyme Expression ◽  
Terminalia Bellirica ◽  
And Oxidative Stress

Excessive oxidative stress plays a critical role in the progression of various diseases. Recently, we showed that Terminalia bellirica (Gaertn.) Roxb. extract (TBE) inhibits inflammatory response and reactive oxygen species (ROS) production in THP-1 macrophages. However, molecular mechanisms underlying anti-inflammatory and antioxidant activities of TBE and its major polyphenolic compounds gallic acid (GA) and ellagic acid (EA) remain unclear. We found that TBE and GA attenuated LPS-induced inflammatory mediator expression, ROS production, and activation of mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-κB) in RAW 264 macrophages. Furthermore, TBE and GA increased antioxidant enzyme expression along with upstream mediators nuclear factor erythroid-2-related factor 2 (Nrf2), Akt, and AMP-activated protein kinase (AMPK). Importantly, knockdown of Nrf2 by siRNA and specific inhibition of Akt and AMPK significantly reduced antioxidant enzyme expression induced by TBE and GA. Finally, in vivo effects on histopathology and gene expression were assessed in tissues collected after intraperitoneal injection of LPS with or without TBE treatment. TBE enhanced antioxidant enzyme expression and improved acute kidney injury in LPS-shock model mice. In conclusion, TBE and GA exert protective effects against inflammation and oxidative stress by suppressing MAPK/NF-κB pathway and by activating Akt/AMPK/Nrf2 pathway. These results suggest that TBE and GA might be effective for the treatment of inflammation-related diseases.

Swainsonine Modulation of Protein Kinase C Activity in Murine Peritoneal Macrophages

1990 ◽  
Vol 2 (10) ◽  
pp. 333-338 ◽  
Author(s):  
Pascal Breton ◽  
Amha Asseffa ◽  
Krzysztof Grzegorzewski ◽  
Steven K. Akiyama ◽  
Sandra L. White ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Peritoneal Macrophages ◽  
Kinase C ◽  
Protein Kinase C Activity ◽  
Murine Peritoneal Macrophages

scholarly journals Differential Bacterial Survival, Replication, and Apoptosis-Inducing Ability of Salmonella Serovars within Human and Murine Macrophages

2000 ◽  
Vol 68 (3) ◽  
pp. 1005-1013 ◽  
Author(s):  
William R. Schwan ◽  
Xiao-Zhe Huang ◽  
Lan Hu ◽  
Dennis J. Kopecko
Keyword(s):  
Typhoid Fever ◽  
Systemic Infection ◽  
Peritoneal Macrophages ◽  
Human Macrophage ◽  
U937 Cells ◽  
Bacterial Survival ◽  
Human Macrophages ◽  
Macrophage Cells ◽  
Serovar Typhimurium ◽  
Murine Peritoneal Macrophages

ABSTRACT Salmonella serovars are associated with human diseases that range from mild gastroenteritis to host-disseminated enteric fever. Human infections by Salmonella enterica serovar Typhi can lead to typhoid fever, but this serovar does not typically cause disease in mice or other animals. In contrast, S. enterica serovar Typhimurium and S. entericaserovar Enteritidis, which are usually linked to localized gastroenteritis in humans and some animal species, elicit a systemic infection in mice. To better understand these observations, multiple strains of each of several chosen serovars of Salmonellawere tested for the ability in the nonopsonized state to enter, survive, and replicate within human macrophage cells (U937 and elutriated primary cells) compared with murine macrophage cells (J774A.1 and primary peritoneal cells); in addition, death of the infected macrophages was monitored. The serovar Typhimurium strains all demonstrated enhanced survival within J774A.1 cells and murine peritoneal macrophages, compared with the significant, almost 100-fold declines in viable counts noted for serovar Typhi strains. Viable counts for serovar Enteritidis either matched the level of serovar Typhi (J774A.1 macrophages) or were comparable to counts for serovar Typhimurium (murine peritoneal macrophages). Apoptosis was significantly higher in J774A.1 cells infected with serovar Typhimurium strain LT2 compared to serovar Typhi strain Ty2. On the other hand, serovar Typhi survived at a level up to 100-fold higher in elutriated human macrophages and 2- to 3-fold higher in U937 cells compared to the serovar Typhimurium and Enteritidis strains tested. Despite the differential multiplication of serovar Typhi during infection of U937 cells, serovar Typhi caused significantly less apoptosis than infections with serovar Typhimurium. These observations indicate variability in intramacrophage survival and host cytotoxicity among the various serovars and are the first to show differences in the apoptotic response of distinctSalmonella serovars residing in human macrophage cells. These studies suggest that nonopsonized serovar Typhimurium enters, multiplies within, and causes considerable, acute death of macrophages, leading to a highly virulent infection in mice (resulting in death within 14 days). In striking contrast, nonopsonized serovar Typhi survives silently and chronically within human macrophages, causing little cell death, which allows for intrahost dissemination and typhoid fever (low host mortality). The type of disease associated with any particular serovar of Salmonellais linked to the ability of that serovar both to persist within and to elicit damage in a specific host's macrophage cells.

Activation of murine peritoneal macrophages by Salmonella typhimurium

1989 ◽  
Vol 26 (1-2) ◽  
pp. 208-210
Author(s):  
J. A. M. Langermans ◽  
P. H. Nibbering ◽  
R. Furth
Keyword(s):  
Salmonella Typhimurium ◽  
Peritoneal Macrophages ◽  
Murine Peritoneal Macrophages
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