Inflammation, Mitochondria and Natural Compounds Together in the Circle of Trust

Abstract

Human diseases are characterized by the perpetuation of an inflammatory condition in which the levels of Reactive Oxygen Species (ROS) are quite high. Excessive ROS production leads to DNA damage, protein carbonylation and lipid peroxidation, conditions that lead to a worsening of inflammatory disorders. In particular, compromised mitochondria sustain a stressful condition in the cell, such that mitochondrial dysfunctions become pathogenic, causing human disorders related to inflammatory reactions. Indeed, the triggered inflammation loses its beneficial properties and turns harmful if dysregulation and dysfunctions are not addressed. Thus, reducing oxidative stress with ROS scavenger compounds has proven to be a successful approach to reducing inflammation. Among these, natural compounds, in particular, polyphenols, alkaloids and coenzyme Q10, thanks to their antioxidant properties, are capable of inhibiting the activation of NF-κB and the expression of target genes, including those involved in inflammation. Even more, clinical trials, and in vivo and in vitro studies have demonstrated the antioxidant and anti-inflammatory effects of phytosomes, which are capable of increasing the bioavailability and effectiveness of natural compounds, and have long been considered an effective non-pharmacological therapy. Therefore, in this review, we wanted to highlight the relationship between inflammation, altered mitochondrial oxidative activity in pathological conditions, and the beneficial effects of phytosomes. To this end, a PubMed literature search was conducted with a focus on various in vitro and in vivo studies and clinical trials from 2014 to 2022.

Preventive Action of Beta-Carotene against the Indoxyl Sulfate-Induced Renal Dysfunction in Male Adult Zebrafish via Regulations of Mitochondrial Inflammatory and β-Carotene Oxygenase-2 Actions

“…The development of oxidative stress also indicates the reduction of SOD2 and GPX1 subsequence decrease in the GSH/GSSG ratio in mitochondria [60]. Moreover, the progress of mitochondrial inflammation, indicated by the accumulation of carbonylated proteins [61], lack of mitochondrial ATP generation, and rising complex I activity level, is an indicator of a lack of mitochondrial metabolic functions, mitochondrial energetics, and antioxidant response [62,63]. In the present study, the exposure of IS (10 mg/L/hour/day; for 4 weeks) showed a significant (p < 0.05) reduction of BCO2, SOD2, and GPX1 activities along with a reduction in GSH/GSSG ratio and ATP contents.…”

UCP2, a Member of the Mitochondrial Uncoupling Proteins: An Overview from Physiological to Pathological Roles

“…These two different pores are placed on the inner and outer mitochondrial membrane, respectively. The mtDNA released in the cytosol acts as a DAMP (damage-associated molecular pattern) molecule, activating the inflammasome and the cGAS-STING complex responsible for proinflammatory molecules, such as interleukin-1β and interleukin-18 and interferon signalling [ 61 , 62 ]. Thus, the antioxidant activities of UCP2 can revert the renal injury aggravated by lipopolysaccharide (LPS), counteracting the inflammation, macrophage infiltration, and the mitochondrial dysfunction linked to oxidative stress [ 35 ].…”

Insomnia in Forensic Detainees: Is Salience Network the Common Pathway for Sleep, Neuropsychiatric, and Neurodegenerative Disorders?

“…Accumulation of senescent cells due to accelerated aging and impaired removal leads to inflammation, a pathology encountered in sleep deprivation, severe mental illness and FTD [ 36 , 37 , 38 ]. Since mitochondria is a key driver of inflammation, dysfunction or loss of these organelles likely account for these pathologies [ 39 , 40 ].…”