Transcutaneous vagus nerve stimulation ameliorates cardiac abnormalities in chronically stressed rats

Agarwal, Vipul; Kaushik, Arjun Singh; Chaudhary, Rishabh; Rehman, Mujeeba; Srivastava, Siddhi; Mishra, Vikas

doi:10.1007/s00210-023-02611-5

Cited by 7 publications

(2 citation statements)

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“…Comparable to fluoxetine, either an enriched environment or acupuncture prevented the stress-induced increase of TNF-α in the HPC, AMY, serum, and spleen of chronically stressed rats [37,85]. The same result was obtained in the serum of rats with taVNS for 2 weeks post-chronic stress [114].…”

Section: Tnf-αsupporting

confidence: 59%

“…These include the following reagents: prebiotic, Eucommiae cortex polysaccharides (Epss) [73]; rice germ with gamma-aminobutyric acid (GABA) [45]; theanine [45]; isofraxidin [39]; hypericum perforatum [109]; serratula coronate [109]; pumpkin extract [110]; RSNP [111]; crocin-1 [111]; bilobalide [112]; TSPG [113]; and B-glucan pretreatment [94,95]. Therapeutic approaches like acupuncture [85] and enriched environment [37] and transcutaneous vagus nerve stimulation (taVNS) [114] decreased IL-6 in either the AMY, HPC, or serum. However, behavioral tests were not completed following acupuncture or taVNS to evaluate the antidepressant-like effects.…”

Section: Il-6mentioning

confidence: 99%

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Chronic Stress-Induced Neuroinflammation: Relevance of Rodent Models to Human Disease

White,

Elias,

Orozco

et al. 2024

IJMS

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The brain is the central organ of adaptation to stress because it perceives and determines threats that induce behavioral, physiological, and molecular responses. In humans, chronic stress manifests as an enduring consistent feeling of pressure and being overwhelmed for an extended duration. This can result in a persistent proinflammatory response in the peripheral and central nervous system (CNS), resulting in cellular, physiological, and behavioral effects. Compounding stressors may increase the risk of chronic-stress-induced inflammation, which can yield serious health consequences, including mental health disorders. This review summarizes the current knowledge surrounding the neuroinflammatory response in rodent models of chronic stress—a relationship that is continually being defined. Many studies investigating the effects of chronic stress on neuroinflammation in rodent models have identified significant changes in inflammatory modulators, including nuclear factor-κB (NF-κB) and toll-like receptors (TLRs), and cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β, and IL-6. This suggests that these are key inflammatory factors in the chronic stress response, which may contribute to the establishment of anxiety and depression-like symptoms. The behavioral and neurological effects of modulating inflammatory factors through gene knockdown (KD) and knockout (KO), and conventional and alternative medicine approaches, are discussed.

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Section: Tnf-αsupporting

confidence: 59%