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Protective Effect of PBCA Nanoparticles Loaded with Thymulin Against the Relapsing-Remitting Form of Experimental Autoimmune Encephalomyelitis in Mice

by Sergey M. Lunin, Maxim O. Khrenov, Olga V. Glushkova, Svetlana B. Parfenyuk, Tatyana V. Novoselova and Elena G. Novoselova

Int. J. Mol. Sci. 2019, 20(21), 5374; https://doi.org/10.3390/ijms20215374 - 29 Oct 2019

Cited by 11 | Viewed by 3645

Abstract

Relapsing–remitting experimental autoimmune encephalomyelitis (rEAE) in mice is a model that closely resembles relapsing–remitting multiple sclerosis in humans. This study aims to investigate a new approach to modulation of the inflammatory response in rEAE mice using a thymic peptide thymulin bound to polybutylcyanoacrylate (PBCA) nanoparticles. PBCA nanoparticles were used to prolong the presence of thymulin in the blood. Cytokine levels in blood were measured by ELISA; NF-κB and SAPK/JNK cascade activation, as well as Hsp72 and p53 protein expression, were measured by Western blotting. Animal health statuses were estimated using severity scores. Results showed that the cytokine response in rEAE was multi-staged: an early phase was accompanied by an increase in plasma interferon-γ, while the interleukin (IL)-17 response was markedly increased at a later stage. The stages were attributed to rEAE induction and maintenance phases. Thymulin significantly alleviated symptoms of rEAE and lowered plasma cytokine levels both in early and later stages of rEAE, and decreased NF-κB and SAPK/JNK cascade activation. Thymulin modulated NF-kappaB pathway activity via site-specific phosphorylation of RelA/p65 protein (at Ser276 and Ser536). The effect of nanoparticle-bound thymulin was more pronounced than the effect of free thymulin. Therefore, PBCA–thymulin can be considered a prospective treatment for this pathology. Full article

(This article belongs to the Special Issue NF-κB and Disease)

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11 pages, 702 KiB

Open AccessReview

The Role of Gene Therapy in Premature Ovarian Insufficiency Management

by Ihor Atabiekov, Elie Hobeika, Ujalla Sheikh, Abdeljabar El Andaloussi and Ayman Al-Hendy

Biomedicines 2018, 6(4), 102; https://doi.org/10.3390/biomedicines6040102 - 1 Nov 2018

Cited by 14 | Viewed by 6039

Abstract

Premature ovarian insufficiency (POI) is a highly prevalent disorder, characterized by the development of menopause before the age of 40. Most cases are idiopathic; however, in some women the cause of this condition (e.g.; anticancer treatment, genetic disorders, and enzymatic defects) could be identified. Although hormone-replacement therapy, the principal therapeutic approach for POI, helps alleviate the related symptoms, this does not effectively solve the issue of fertility. Assisted reproductive techniques also lack efficacy in these women. Thus, an effective approach to manage patients with POI is highly warranted. Several mechanisms associated with POI have been identified, including the lack of function of the follicle-stimulating hormone (FSH) receptor, alterations in apoptosis control, mutations in Sal-like 4 genes, and thymulin or basonuclin-1 deficiency. The above mentioned may be good targets for gene therapy in order to correct defects leading to POI. The goal of this review is to summarize current experiences on POI studies that employed gene therapy, and to discuss possible future directions in this field. Full article

(This article belongs to the Special Issue Pathogenesis, Diagnosis and Therapy of Ovarian Disorders and Infertility)

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