scholarly journals Dietary L-citrulline influences body temperature and inflammatory responses during nitric oxide synthase inhibition and endotoxin challenge in chickens

Stress ◽  
2021 ◽  
pp. 1-33
Author(s):  
Victoria Anthony Uyanga ◽  
Jingpeng Zhao ◽  
Xiaojuan Wang ◽  
Hongchao Jiao ◽  
Okanlawon M. Onagbesan ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Body Temperature ◽  
Nitric Oxide Synthase ◽  
Inflammatory Responses ◽  
Endotoxin Challenge ◽  
Oxide Synthase

scholarly journals AR Deficiency Inhibits LPS-induced M1 Response in Macrophages by Activating Autophagy

2020 ◽  
Author(s):  
Peng Cheng ◽  
Jianwei Xie ◽  
Zhiyong Liu ◽  
Jian Wang
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inflammatory Responses ◽  
Macrophage Polarization ◽  
Critical Role ◽  
Transcriptional Level ◽  
Mrna Levels ◽  
M1 Polarization ◽  
M1 Macrophage ◽  
Oxide Synthase

Abstract Macrophage M1 polarization mediates inflammatory responses and tissue damage. Recently, aldose reductase (AR) has been shown to play a critical role in of M1 polarization in macrophages. However, the underlying mechanisms are unknown. Here, we demonstrated, for the first time, that AR deficiency repressed the induction of inducible nitric oxide synthase in lipopolysaccharide (LPS)-stimulated macrophages via activation of autophagy. This suppression was related to a defect in the inhibitor of nuclear factor κB (NF-κB) kinase (IKK) complex in the classical NF-κB pathway. However, the mRNA levels of the IKKβ and IKKγ were not reduced in LPS-treated AR knockout (KO) macrophages, indicating that their proteins were downregulated at the post-transcriptional level. We discovered that LPS stimuli induced the recruitment of more beclin1 and increased autophagosome formation in AR-deficient macrophages. Blocking autophagy by 3-methyladenine and ammonium chloride treatment restored IKKβ and IKKγ protein levels and increased nitric oxide synthase production in LPS-stimulated AR-deficient macrophages. More assembled IKKβ and IKKγ undergo ubiquitination and recruit the autophagic adaptor p62 in LPS-induced AR KO macrophages, promoting their delivery to autophagosomes and lysosomes. Collectively, these findings suggest that AR deficiency involves in the regulation of NF-κB signaling, and extends the role of selective autophagy in fine-tuned M1 macrophage polarization.

scholarly journals Ghrelin Protects against the Detrimental Consequences ofPorphyromonas gingivalis-Induced Akt Inactivation through S-Nitrosylation on Salivary Mucin Synthesis

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Bronislaw L. Slomiany ◽  
Amalia Slomiany
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inflammatory Responses ◽  
Peptide Hormone ◽  
Inos Expression ◽  
Akt Kinase ◽  
Akt Activation ◽  
Mucin Synthesis ◽  
Salivary Mucin ◽  
Oxide Synthase

Disturbances in nitric oxide synthase isozyme system and the impairment in salivary mucin synthesis are well-recognized features associated with oral mucosal inflammatory responses to periodontopathic bacterium,P. gingivalis. In this study, using rat sublingual gland acinar cells, we report thatP. gingivalisLPS-induced impairment in mucin synthesis and associated suppression in Akt kinase activity were accompanied by a decrease in constitutive nitric oxide synthase (cNOS) activity and an induction in inducible nitric oxide synthase (iNOS) expression. The LPS effect on Akt inactivation was manifested in the kinase S-nitrosylation and a decrease in its phosphorylation at Ser473. Further, we demonstrate that a peptide hormone, ghrelin, countered the LPS-induced impairment in mucin synthesis. This effect of ghrelin was reflected in the suppression of iNOS and the increase in Akt activation, associated with the loss in S-nitrosylation and the increase in phosphorylation, as well as cNOS activation through phosphorylation. Our findings suggest that induction in iNOS expression byP. gingivalis-LPS leads to Akt kinase inactivation through S-nitrosylation that detrimentally impacts cNOS activation through phosphorylation as well as mucin synthesis. We also show that the countering effect of ghrelin onP. gingivalis-induced impairment in mucin synthesis is associated with Akt activation through phosphorylation.

Inhibitors of nitric oxide synthesis block cold-induced thermogenesis in rats

2003 ◽  
Vol 81 (8) ◽  
pp. 834-838 ◽  
Author(s):  
Peter R Kamerman ◽  
Helen P Laburn ◽  
Duncan Mitchell
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Body Temperature ◽  
Nitric Oxide Synthase ◽  
Metabolic Rate ◽  
Water Loss ◽  
T Test ◽  
Evaporative Water Loss ◽  
Evaporative Water ◽  
Oxide Synthase

N-nitro-L-arginine methyl ester (L-NAME), an unspecific nitric oxide synthase inhibitor, was administered to individually caged Sprague–Dawley rats exposed to cold (18°C) and thermoneutral (30°C) environmental temperatures during the active phase of the animals' circadian cycle. Unrestrained rats were administered intraperitoneal injections of 100 mg·kg–1 L-NAME or 1 mL·kg–1 saline. Telemetry was used to measure abdominal temperature. On a separate occasion, metabolic rate and evaporative water loss were measured using indirect calorimetery, before and after the injection of 100 mg·kg–1 L-NAME, in rats exposed to the two environments. Injection of L-NAME had no significant effect on body temperature, metabolic rate, or evaporative water loss in rats exposed to the 30°C environment. In the 18°C environment, L-NAME injection caused a prolonged fall in body temperature (F(1,12) = 17.43, P = 0.001) and a significant decrease in metabolic rate (Student's t test, P = 0.001) and evaporative water loss (one-sample t test, P = 0.04). Therefore, the effects that systemic injection of L-NAME has on body temperature are dependent on environmental temperature, with nitric oxide synthase inhibition seemingly preventing the metabolic component of cold defence.Key words: N-nitro-L-arginine methyl ester, thermoregulation, telemetry, oxygen consumption.

scholarly journals Acute thermal stress promotes morphological and molecular changes in the heart of broiler chickens

2020 ◽  
Vol 9 (8) ◽  
pp. e63985059
Author(s):  
Kariny Ferreira Moreira ◽  
Camila Quaglio Neves ◽  
Stephanie Carvalho Borges ◽  
Ana Paula Del Vesco ◽  
Maria Ida Bonini Ravanelli Speziali ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Thermal Stress ◽  
Body Temperature ◽  
Nitric Oxide Synthase ◽  
Angiotensin Converting Enzyme ◽  
Converting Enzyme ◽  
Molecular Changes ◽  
Transfer Protein ◽  
Aortic Artery ◽  
Oxide Synthase

This study aimed to understand the possible effects of acute thermal stress (32ºC, 12 hours) on body temperature using two measurement methods (via probe and rectal), on the morphometric aspects of the heart and aortic artery, on gene expression (superoxide dismutase, glutathione peroxidase-3, nitric oxide synthase, angiotensin-converting enzyme and esterified cholesterol transfer protein), inflammatory parameters (myeloperoxidase and N-acetylglycosaminidase), oxidative stress parameters and nitrite levels in broilers (Cobb 500) at 42 days of age.  36 broilers with 42 days of age were used, distributed in a 2x2 factorial scheme: two thermal environments (comfort at 18ºC and stress at 32ºC) and two methods of measuring body temperature (via probe and rectal). Thermal stress triggered an increase in body temperature regardless of the measurement method. There was a significant effect on the thickness of the aortic artery wall and on the lateral lateral and posterior antero diameters (P <0.05). Likewise, there was a difference in the dosages of lipid hydroperoxides, in the quantification of reactive oxygen species and in the dosage of nitrite (P <0.05). The quantification of the mRNA of the induced nitric oxide synthase, angiotensin-converting enzyme and esterified cholesterol transfer protein genes were significantly higher in animals subjected to heat stress. Thus, it can be concluded that acute thermal stress was able to promote several morphological and molecular changes in the heart and aorta artery of broilers.

scholarly journals Nitric oxide synthase neurons in the preoptic hypothalamus are sleep-active and contribute to regulating NREM and REM sleep and lowering body temperature.

2021 ◽  
Author(s):  
Edward C Harding ◽  
Wei Ba ◽  
Reesha Zahir ◽  
Xiao Yu ◽  
Raquel Yustos ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Body Temperature ◽  
Nitric Oxide Synthase ◽  
Rem Sleep ◽  
Active Phase ◽  
Nrem Sleep ◽  
Dark Phase ◽  
Dark Light ◽  
Active Population ◽  
Oxide Synthase

When mice are exposed to external warmth, nitric oxide synthase (NOS1) neurons in the median and medial preoptic (MnPO/MPO) hypothalamus induce sleep and concomitant body cooling. However, how these neurons regulate baseline sleep and body temperature is unknown. Using calcium photometry, we show that NOS1 neurons in MnPO/MPO are predominantly NREM active. This is the first instance of a predominantly NREM-active population in the PO area, or to our knowledge, elsewhere in the brain. In addition to releasing nitric oxide, NOS1 neurons in MnPO/MPO can release GABA, glutamate and peptides. We expressed tetanus-toxin light-chain in MnPO/MPO NOS1 cells to reduce vesicular release of transmitters. This induced changes in sleep structure: over 24 hours, mice had less NREM sleep in their dark (active) phase, and more NREM sleep in their light (sleep) phase. REM sleep episodes in the dark phase were longer, and there were fewer REM transitions between other vigilance states. REM sleep had less theta power. Mice with synaptically-blocked MnPO/MPO NOS1 neurons were also warmer. In particular, mice were warmer than control mice at the dark-light transition (ZT0), as well as during the dark phase siesta (ZT16-20), where there is usually a body temperature dip. Also, at this siesta point of cooled body temperature, mice usually have more NREM, but mice with synaptically-blocked MnPO/MPO NOS1 cells showed reduced NREM sleep at this time. Overall, MnPO/MPO NOS1 neurons promote both NREM and REM sleep and contribute to chronically lowering body temperature, particularly at transitions where the mice normally enter NREM sleep.

scholarly journals Nitric Oxide Synthase Neurons in the Preoptic Hypothalamus Are NREM and REM Sleep-Active and Lower Body Temperature

2021 ◽  
Vol 15 ◽  
Author(s):  
Edward C. Harding ◽  
Wei Ba ◽  
Reesha Zahir ◽  
Xiao Yu ◽  
Raquel Yustos ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Body Temperature ◽  
Nitric Oxide Synthase ◽  
Rem Sleep ◽  
Active Phase ◽  
Nrem Sleep ◽  
Dark Phase ◽  
Dark Light ◽  
Body Cooling ◽  
Oxide Synthase

When mice are exposed to external warmth, nitric oxide synthase (NOS1) neurons in the median and medial preoptic (MnPO/MPO) hypothalamus induce sleep and concomitant body cooling. However, how these neurons regulate baseline sleep and body temperature is unknown. Using calcium photometry, we show that NOS1 neurons in MnPO/MPO are predominantly NREM and REM active, especially at the boundary of wake to NREM transitions, and in the later parts of REM bouts, with lower activity during wakefulness. In addition to releasing nitric oxide, NOS1 neurons in MnPO/MPO can release GABA, glutamate and peptides. We expressed tetanus-toxin light-chain in MnPO/MPO NOS1 cells to reduce vesicular release of transmitters. This induced changes in sleep structure: over 24 h, mice had less NREM sleep in their dark (active) phase, and more NREM sleep in their light (sleep) phase. REM sleep episodes in the dark phase were longer, and there were fewer REM transitions between other vigilance states. REM sleep had less theta power. Mice with synaptically blocked MnPO/MPO NOS1 neurons were also warmer than control mice at the dark-light transition (ZT0), as well as during the dark phase siesta (ZT16-20), where there is usually a body temperature dip. Also, at this siesta point of cooled body temperature, mice usually have more NREM, but mice with synaptically blocked MnPO/MPO NOS1 cells showed reduced NREM sleep at this time. Overall, MnPO/MPO NOS1 neurons promote both NREM and REM sleep and contribute to chronically lowering body temperature, particularly at transitions where the mice normally enter NREM sleep.

Sign in / Sign up

Export Citation Format

Share Document