The immunomodulatory mechanism of brain injury induced by hyperhomocysteinemia in spontaneously hypertensive rats

Wang, Lin; Zhou, Xin; Li, Xin

doi:10.1002/jcb.28217

Cited by 10 publications

(3 citation statements)

References 56 publications

(89 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Elevation of Hcy level during chronic methionine administration to rats was found to decrease the plasma concentration of IL-10 but there was no effect on the expression of this anti-inflammatory cytokine in brain tissues [ 35 ]. The same authors showed that the IL-10 mRNA levels were manifestly downregulated in the brain of spontaneously hypertensive rats with elevated blood concentration of Hcy [ 36 ]. Another study demonstrated that HHC decreased TNF-α and increased IL-1β gene expression in the striatum of rats while in the cerebellum, expression of TNF-α, IL-1β, IL-10, and TGF-β was increased [ 37 ].…”

Section: Discussionmentioning

confidence: 99%

Prenatal Hyperhomocysteinemia Induces Glial Activation and Alters Neuroinflammatory Marker Expression in Infant Rat Hippocampus

Shcherbitskaia

Vasilev

Milyutina

et al. 2021

Cells

View full text Add to dashboard Cite

Maternal hyperhomocysteinemia is one of the common complications of pregnancy that causes offspring cognitive deficits during postnatal development. In this study, we investigated the effect of prenatal hyperhomocysteinemia (PHHC) on inflammatory, glial activation, and neuronal cell death markers in the hippocampus of infant rats. Female Wistar rats received L-methionine (0.6 g/kg b.w.) by oral administration during pregnancy. On postnatal days 5 and 20, the offspring’s hippocampus was removed to perform histological and biochemical studies. After PHHC, the offspring exhibited increased brain interleukin-1β and interleukin-6 levels and glial activation, as well as reduced anti-inflammatory interleukin-10 level in the hippocampus. Additionally, the activity of acetylcholinesterase was increased in the hippocampus of the pups. Exposure to PHHC also resulted in the reduced number of neurons and disrupted neuronal ultrastructure. At the same time, no changes in the content and activity of caspase-3 were found in the hippocampus of the pups. In conclusion, our findings support the hypothesis that neuroinflammation and glial activation could be involved in altering the hippocampus cellular composition following PHHC, and these alterations could be associated with cognitive disorders later in life.

show abstract

Section: Discussionmentioning

confidence: 99%

Prenatal Hyperhomocysteinemia Induces Glial Activation and Alters Neuroinflammatory Marker Expression in Infant Rat Hippocampus

Shcherbitskaia

Vasilev

Milyutina

et al. 2021

Cells

View full text Add to dashboard Cite

show abstract

“…Thus, mild hyperhomocysteinemia in AD may not be associated with inflammatory reactions. Notoriously, hyperhomocysteinemia-induced brain injury and disruption of BBB are mediated by the release of pro-inflammatory cytokine and immunomodulatory dysfunction to protect the injured brain (Zhang et al 2019 ).…”

Section: Hyperhomocysteinemia and Immunoinflammatory Response In Pdmentioning

confidence: 99%

Parkinson’s Disease Risk and Hyperhomocysteinemia: The Possible Link

et al. 2023

View full text Add to dashboard Cite

Parkinson’s disease (PD) is one of the most common degenerative brain disorders caused by the loss of dopaminergic neurons in the substantia nigra (SN). Lewy bodies and -synuclein accumulation in the SN are hallmarks of the neuropathology of PD. Due to lifestyle changes and prolonged L-dopa administration, patients with PD frequently have vitamin deficiencies, especially folate, vitamin B6, and vitamin B12. These disorders augment circulating levels of Homocysteine with the development of hyperhomocysteinemia, which may contribute to the pathogenesis of PD. Therefore, this review aimed to ascertain if hyperhomocysteinemia may play a part in oxidative and inflammatory signaling pathways that contribute to PD development. Hyperhomocysteinemia is implicated in the pathogenesis of neurodegenerative disorders, including PD. Hyperhomocysteinemia triggers the development and progression of PD by different mechanisms, including oxidative stress, mitochondrial dysfunction, apoptosis, and endothelial dysfunction. Particularly, the progression of PD is linked with high inflammatory changes and systemic inflammatory disorders. Hyperhomocysteinemia induces immune activation and oxidative stress. In turn, activated immune response promotes the development and progression of hyperhomocysteinemia. Therefore, hyperhomocysteinemia-induced immunoinflammatory disorders and abnormal immune response may aggravate abnormal immunoinflammatory in PD, leading to more progression of PD severity. Also, inflammatory signaling pathways like nuclear factor kappa B (NF-κB) and nod-like receptor pyrin 3 (NLRP3) inflammasome and other signaling pathways are intricate in the pathogenesis of PD. In conclusion, hyperhomocysteinemia is involved in the development and progression of PD neuropathology either directly via induction degeneration of dopaminergic neurons or indirectly via activation of inflammatory signaling pathways.

show abstract

“…Long-term use of LC40 could treat and prevent intestinal flora disorders, and restore the balance of altered helper Th17 and Tregs in mesenteric lymph nodes (MLN) ( Toral et al., 2018 ). Th17 cells produce interleukin-17 (IL-17), which has powerful pro-inflammatory effects, and the IL-17 content in the plasma of hypertensive patients remains at a high level ( Zhang et al., 2019 ). Moreover, IL-17 is associated with Ang II, which is an important mediator of Ang II-induced hypertension ( Basile et al., 2021 ).…”

Section: Probiotic Adjuvant Therapy For Hypertensionmentioning

confidence: 99%

Probiotics: functional food ingredients with the potential to reduce hypertension

Chen

Liang²,

Liu

et al. 2023

Front. Cell. Infect. Microbiol.

View full text Add to dashboard Cite

Hypertension is an increasingly pressing public health concern across the globe. It can be triggered by a variety of factors such as age and diet, as well as the stress of modern life. The traditional treatment of hypertension includes calcium ion blockers, angiotensin II receptor inhibitors and β-receptor blockers, but these drugs have at least some side effects. Recent studies have revealed that intestinal flora plays a vital role in maintaining and promoting human health. This is due to the type and amount of probiotics present in the flora. Probiotics can reduce hypertension symptoms through four mechanisms: regulating vascular oxidative stress, producing short-chain fatty acids, restoring endothelial cell function, and reducing inflammation. It has been reported that certain functional foods, using probiotics as their raw material, can modify the composition of intestinal flora, thus regulating hypertension symptoms. Consequently, utilizing the probiotic function of probiotics in conjunction with the properties of functional foods to treat hypertension is a novel, side-effect-free treatment method. This study seeks to summarize the various factors that contribute to hypertension, the mechanism of probiotics in mitigating hypertension, and the fermented functional foods with probiotic strains, in order to provide a basis for the development of functional foods which utilize probiotics as their raw material and may have the potential to reduce hypertension.

show abstract

The immunomodulatory mechanism of brain injury induced by hyperhomocysteinemia in spontaneously hypertensive rats

Cited by 10 publications

References 56 publications

Prenatal Hyperhomocysteinemia Induces Glial Activation and Alters Neuroinflammatory Marker Expression in Infant Rat Hippocampus

Prenatal Hyperhomocysteinemia Induces Glial Activation and Alters Neuroinflammatory Marker Expression in Infant Rat Hippocampus

Parkinson’s Disease Risk and Hyperhomocysteinemia: The Possible Link

Probiotics: functional food ingredients with the potential to reduce hypertension

Contact Info

Product

Resources

About