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The Effects of β-Funaltrexamine on L...

Hodge, Karissa,

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The Effects of β-Funaltrexamine on Lipopolysaccharide-Induced Inflammation and Behavior /

Record Type:	Electronic resources : Monograph/item
Title/Author:	The Effects of β-Funaltrexamine on Lipopolysaccharide-Induced Inflammation and Behavior // Karissa Hodge.
Author:	Hodge, Karissa,
Description:	1 electronic resource (149 pages)
Notes:	Source: Dissertations Abstracts International, Volume: 86-01, Section: B.
Contained By:	Dissertations Abstracts International86-01B.
Subject:	Pharmacology. -
Online resource:	https://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=31239890
ISBN:	9798383216941

The Effects of β-Funaltrexamine on Lipopolysaccharide-Induced Inflammation and Behavior /
Hodge, Karissa,

The Effects of β-Funaltrexamine on Lipopolysaccharide-Induced Inflammation and Behavior /Karissa Hodge. - 1 electronic resource (149 pages)

Source: Dissertations Abstracts International, Volume: 86-01, Section: B.

Inflammation plays a crucial role in the development, progression, and severity of many prevalent systemic and neurological pathologies. A growing body of evidence has found that inflammation is a key aspect of cardiovascular disease, autoimmune disorders, cancer, neurodegenerative diseases, and neuropsychiatric conditions. Consequently, there is a critical need to develop targeted pharmaceuticals to mitigate systemic inflammation and inflammation-induced behavioral deficits. Our lab has previously demonstrated that acute β-FNA has selective anti-inflammatory effects in normal human astrocytes and reduces systemic inflammatory mediators and anxiety- and sickness-like behavior in male mice, predominantly through inhibition of p38 MAPK and NF-κB. The purpose of this study was to extend our knowledge of the cell-specific effects of acute β-FNA treatment using microglial cells, as well as study chronic pre-treatment effects on systemic inflammation and inflammation-induced behavioral deficits using a preclinical model. BV2 murine microglial cells were co-incubated with β-FNA and LPS at various times, while osmotic drug pumps were surgically inserted into mice that continually dispensed β-FNA for six days prior to LPS injection. Depressive-, anxiety-, and sickness-like behaviors were measured 24h after LPS injection, and then mice were terminated, and plasma, frontal cortex, hippocampus, and spleen tissues were harvested. CCL2, CXCL10, and IL-1β levels were measured in cell supernatant, CCL2 and CXCL10 were measured in frontal cortex, hippocampus, and spleen tissues, and IL-1β and corticosterone were measured in mouse plasma via ELISA. IDO1 and NLRP3 transcription were quantified via RT-qPCR from whole cell lysates and the afore-mentioned tissue homogenates. Additionally, p38 MAPK and STAT1 were quantified via Western blots in whole cell lysates. Acute β-FNA selectively reduced CCL2 and paradoxically potentiated LPS-driven IL-1β in BV2 cells, while exhibiting no effect on p38 MAPK, STAT1, NLRP3, or IDO1. Behavioral deficits were predominantly correlated with neuroinflammatory levels of CCL2, CXCL10, NLRP3, and IDO1. Additionally, chronic β-FNA pre-treatment greatly reduced systemic levels of CCL2 and CXCL10 and inhibited or abolished anxiety- and sickness-like behaviors. Interestingly, β-FNA increased frontal cortex inflammation and anxiety-like behavior under control conditions. Consequently, these studies provide additional insight into the actions and therapeutic potential of β-FNA and underscore areas that need further investigation.

English

ISBN: 9798383216941Subjects--Topical Terms:

634543
Pharmacology.
Subjects--Index Terms:

β-funaltrexamine

The Effects of β-Funaltrexamine on Lipopolysaccharide-Induced Inflammation and Behavior /
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502 $b Ph.D. $c Oklahoma State University $d 2024.
520 $a Inflammation plays a crucial role in the development, progression, and severity of many prevalent systemic and neurological pathologies. A growing body of evidence has found that inflammation is a key aspect of cardiovascular disease, autoimmune disorders, cancer, neurodegenerative diseases, and neuropsychiatric conditions. Consequently, there is a critical need to develop targeted pharmaceuticals to mitigate systemic inflammation and inflammation-induced behavioral deficits. Our lab has previously demonstrated that acute β-FNA has selective anti-inflammatory effects in normal human astrocytes and reduces systemic inflammatory mediators and anxiety- and sickness-like behavior in male mice, predominantly through inhibition of p38 MAPK and NF-κB. The purpose of this study was to extend our knowledge of the cell-specific effects of acute β-FNA treatment using microglial cells, as well as study chronic pre-treatment effects on systemic inflammation and inflammation-induced behavioral deficits using a preclinical model. BV2 murine microglial cells were co-incubated with β-FNA and LPS at various times, while osmotic drug pumps were surgically inserted into mice that continually dispensed β-FNA for six days prior to LPS injection. Depressive-, anxiety-, and sickness-like behaviors were measured 24h after LPS injection, and then mice were terminated, and plasma, frontal cortex, hippocampus, and spleen tissues were harvested. CCL2, CXCL10, and IL-1β levels were measured in cell supernatant, CCL2 and CXCL10 were measured in frontal cortex, hippocampus, and spleen tissues, and IL-1β and corticosterone were measured in mouse plasma via ELISA. IDO1 and NLRP3 transcription were quantified via RT-qPCR from whole cell lysates and the afore-mentioned tissue homogenates. Additionally, p38 MAPK and STAT1 were quantified via Western blots in whole cell lysates. Acute β-FNA selectively reduced CCL2 and paradoxically potentiated LPS-driven IL-1β in BV2 cells, while exhibiting no effect on p38 MAPK, STAT1, NLRP3, or IDO1. Behavioral deficits were predominantly correlated with neuroinflammatory levels of CCL2, CXCL10, NLRP3, and IDO1. Additionally, chronic β-FNA pre-treatment greatly reduced systemic levels of CCL2 and CXCL10 and inhibited or abolished anxiety- and sickness-like behaviors. Interestingly, β-FNA increased frontal cortex inflammation and anxiety-like behavior under control conditions. Consequently, these studies provide additional insight into the actions and therapeutic potential of β-FNA and underscore areas that need further investigation.
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590 $a School code: 0664
650 4 $a Pharmacology. $3 634543
650 4 $a Physiology. $3 518431
650 4 $a Pathology. $3 643180
650 4 $a Biomedical engineering. $3 535387
653 $a β-funaltrexamine
653 $a Inflammation
653 $a Lipopolysaccharide
653 $a LPS injection
653 $a Neuroinflammation
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690 $a 0571
690 $a 0541
710 2 $a Oklahoma State University. $b Biomedical Sciences. $e degree granting institution. $3 3827134
720 1 $a Davis, Randall $e degree supervisor.
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791 $a Ph.D.
792 $a 2024
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