Effect of Therapeutic Plasma Exchange on Plasma Constituents in Neurointensive Care Unit Patients: A Retrospective Study

Srinivas, Deepti; Sriganesh, Kamath; Chakrabarti, Dhritiman; Venkateswaran, Pavithra

doi:10.1055/s-0041-1734412

Cited by 1 publication

(1 citation statement)

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“…TPE techniques using peripheral venous access and high transmembrane pressure cause hemolysis during the procedure [71], which could contribute to BACH1 inhibition as well. Likewise, the significant decrease in plasma proteins and other plasma constituents observed during TPE [72] could contribute to amino acid losses, a well-known inducer of ATF4 [73]. Thus, TPE could modulate HO-1 expression indirectly at multiple levels.…”

Section: Nrf2 Pathway In Msmentioning

confidence: 99%

Oxidative Stress and the Nuclear Factor Erythroid 2-Related Factor 2 (Nrf2) Pathway in Multiple Sclerosis: Focus on Certain Exogenous and Endogenous Nrf2 Activators and Therapeutic Plasma Exchange Modulation

Tonev,

Momchilova

2023

IJMS

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The pathogenesis of multiple sclerosis (MS) suggests that, in genetically susceptible subjects, T lymphocytes undergo activation in the peripheral compartment, pass through the BBB, and cause damage in the CNS. They produce pro-inflammatory cytokines; induce cytotoxic activities in microglia and astrocytes with the accumulation of reactive oxygen species, reactive nitrogen species, and other highly reactive radicals; activate B cells and macrophages and stimulate the complement system. Inflammation and neurodegeneration are involved from the very beginning of the disease. They can both be affected by oxidative stress (OS) with different emphases depending on the time course of MS. Thus, OS initiates and supports inflammatory processes in the active phase, while in the chronic phase it supports neurodegenerative processes. A still unresolved issue in overcoming OS-induced lesions in MS is the insufficient endogenous activation of the Nuclear Factor Erythroid 2-Related Factor 2 (Nrf2) pathway, which under normal conditions plays an essential role in mitochondria protection, OS, neuroinflammation, and degeneration. Thus, the search for approaches aiming to elevate endogenous Nrf2 activation is capable of protecting the brain against oxidative damage. However, exogenous Nrf2 activators themselves are not without drawbacks, necessitating the search for new non-pharmacological therapeutic approaches to modulate OS. The purpose of the present review is to provide some relevant preclinical and clinical examples, focusing on certain exogenous and endogenous Nrf2 activators and the modulation of therapeutic plasma exchange (TPE). The increased plasma levels of nerve growth factor (NGF) in response to TPE treatment of MS patients suggest their antioxidant potential for endogenous Nrf2 enhancement via NGF/TrkA/PI3K/Akt and NGF/p75NTR/ceramide-PKCζ/CK2 signaling pathways.

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Section: Nrf2 Pathway In Msmentioning

confidence: 99%