Administration of α-lipoic acid and silymarin attenuates aggression by modulating endocrine, oxidative stress and inflammatory pathways in mice

Karim, Adnan; F, Anwar; Saleem, Uzma; Fatima, Saniya; Ismail, Tariq; Obaidullah, Ahmad J.; Khayat, Rana O.; Alqahtani, Moneerah J.; Alsharif, Ifat; Khan, Haroon; Vargas-De-La-Cruz, Celia; Shah, Muhammad Ajmal

doi:10.1007/s11011-023-01258-8

Cited by 3 publications

(2 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The oral administration of SB (100 mg/kg) was demonstrated to protect against MPTP-induced neurotoxicity by reducing the levels of pro-inflammatory cytokines (TNFα, IL-1β and IL-6) in the striatum and substantia nigra and increasing anti-inflammatory cytokine (IL-10 and IL-4) levels in the substantia nigra in mice [173]. The administration of silymarin (200 mg/kg) to aggression-induced mice was indicated to attenuate inflammation (decreased serum IL-6 and TNF-α) and decrease oxidative stress (GSH, CAT and SOD) in the mouse brain [174]. The lower SM dose (100 mg/kg) also improved AO defences in the brain and decreased TNF-α levels in serum but did not affect the IL-6 concentration in serum.…”

Section: Other In Vivo Model Systems and Disease Statesmentioning

confidence: 97%

Silymarin and Inflammation: Food for Thoughts

Surai,

Earle-Payne

2024

Antioxidants

View full text Add to dashboard Cite

Inflammation is a vital defense mechanism, creating hostile conditions for pathogens, preventing the spread of tissue infection and repairing damaged tissues in humans and animals. However, when inflammation resolution is delayed or compromised as a result of its misregulation, the process proceeds from the acute phase to chronic inflammation, leading to the development of various chronic illnesses. It is proven that redox balance disturbances and oxidative stress are among major factors inducing NF-κB and leading to over-inflammation. Therefore, the anti-inflammatory properties of various natural antioxidants have been widely tested in various in vitro and in vivo systems. Accumulating evidence indicates that silymarin (SM) and its main constituent silibinin/silybin (SB) have great potential as an anti-inflammation agent. The main anti-inflammatory mechanism of SM/SB action is attributed to the inhibition of TLR4/NF-κB-mediated signaling pathways and the downregulated expression of pro-inflammatory mediators, including TNF-α, IL-1β, IL-6, IL-12, IL-23, CCL4, CXCL10, etc. Of note, in the same model systems, SM/SB was able to upregulate anti-inflammatory cytokines (IL-4, IL-10, IL-13, TGF-β, etc.) and lipid mediators involved in the resolution of inflammation. The inflammatory properties of SM/SB were clearly demonstrated in model systems based on immune (macrophages and monocytes) and non-immune (epithelial, skin, bone, connective tissue and cancer) cells. At the same time, the anti-inflammatory action of SM/SB was confirmed in a number of in vivo models, including toxicity models, nonalcoholic fatty liver disease, ischemia/reperfusion models, stress-induced injuries, ageing and exercising models, wound healing and many other relevant model systems. It seems likely that the anti-inflammatory activities of SM/SB are key elements on the health-promoting properties of these phytochemicals.

show abstract

Section: Other In Vivo Model Systems and Disease Statesmentioning

confidence: 97%

Silymarin and Inflammation: Food for Thoughts

Surai,

Earle-Payne

2024

Antioxidants

View full text Add to dashboard Cite

show abstract

“…The aggressor cat and the bullied cat are at risk for oxidative stress and neuroinflammation ( 72 ). When aggressive mice are treated with antioxidants, biomarkers for oxidative stress, pro-inflammatory cytokines and aggressive behaviors decreased ( 73 ). The less dominant cat is at risk for depression, just as their human counterparts ( 74–76 ).…”

Section: Introductionmentioning

confidence: 99%

Stress and the domestic cat: have humans accidentally created an animal mimic of neurodegeneration?

Niesman

2024

Front. Neurol.

View full text Add to dashboard Cite

Many neurodegenerative diseases (NDD) appear to share commonality of origin, chronic ER stress. The endoplasmic reticulum (ER) is a dynamic organelle, functioning as a major site of protein synthesis and protein posttranslational modifications, required for proper folding. ER stress can occur because of external stimuli, such as oxidative stress or neuroinflammatory cytokines, creating the ER luminal environment permissive for the accumulation of aggregated and misfolded proteins. Unresolvable ER stress upregulates a highly conserved pathway, the unfolded protein response (UPR). Maladaptive chronic activation of UPR components leads to apoptotic neuronal death. In addition to other factors, physiological responses to stressors are emerging as a significant risk factor in the etiology and pathogenesis of NDD. Owned cats share a common environment with people, being exposed to many of the same stressors as people and additional pressures due to their “quasi” domesticated status. Feline Cognitive Dysfunction Syndrome (fCDS) presents many of the same disease hallmarks as human NDD. The prevalence of fCDS is rapidly increasing as more people welcome cats as companions. Barely recognized 20 years ago, veterinarians and scientists are in infancy stages in understanding what is a very complex disease. This review will describe how cats may represent an unexplored animal mimetic phenotype for human NDD with stressors as potential triggering mechanisms. We will consider how multiple variations of stressful events over the short-life span of a cat could affect neuronal loss or glial dysfunction and ultimately tip the balance towards dementia.

show abstract