4 research outputs found
Antioxidant potential of the polyherbal formulation âImmuPlusâ, a nutritional supplement for horses
In order to counteract harmful effects of oxidative stress due to pathological conditions or physical exercise, horses are often
administered dietary supplements having supposed high antioxidant activities. The aim of the present study was to identify the
in vitro antioxidant potential of âImmuPlusâ, a polyherbal formulation (Global Herbs LTD, Chichester,West Sussex, Great Britain),
containing three medicinal plants (Withania somnifera, Tinospora cordifolia, and Emblica officinalis), known in Ayurveda for their
use in human disease treatment. Extracts obtained by different solvents (water,methanol, ethanol, acetone, and hexane) were tested
for total antioxidant capacity, total reducing power, scavenging activity against DPPH radical, and total polyphenol and flavonoid
contents. Our results showed that, except as regards hexane, all the used solvents are able to extract compounds having high
antioxidant activity, even when compared to ascorbic acid. Regression analysis showed significant correlations between antioxidant
properties and polyphenol/flavonoid contents, indicating the latter, known for their beneficial effects on health of human and animal
beings, as major components responsible for the strong antioxidant capacities.Moreover, obtained results suggest the effective role
of the polyherbal mixture as good source of antioxidants in horses
EDA-ID and IP, Two Faces of the Same Coin: How the Same IKBKG / NEMO Mutation Affecting the NF-B Pathway Can Cause Immunodeficiency and/or Inflammation
Anhidrotic Ectodermal Dysplasia with ImmunoDeficiency (EDA-ID, OMIM 300291) and Incontinentia Pigmenti (IP, OMIM 308300) are two rare diseases, caused by mutations of the IKBKG/NEMO gene. The protein NEMO/IKKÎł is essential for the NF-ÎșB activation pathway, involved in a variety of physiological and cellular processes, such as immunity, inflammation, cell proliferation, and survival. A wide spectrum of IKBKG/NEMO mutations have been identified so far, and, on the basis of their effect on NF-ÎșB activation, they are considered hypomorphic or amorphic (loss of function) mutations. IKBKG/NEMO hypomorphic mutations, reducing but not abolishing NF-ÎșB activation, have been identified in EDA-ID and IP patients. Instead, the amorphic mutations, abolishing NF-ÎșB activation by complete IKBKG/NEMO gene silencing, cause only IP. Here, we present an overview of IKBKG/NEMO mutations in EDA-ID and IP patients and describe similarities and differences between the clinical/immunophenotypic and genetic aspects, highlighting any T and B lymphocyte defect, and paying particular attention to the cellular and molecular defects that underlie the pathogenesis of both diseases