Corrigendum: Characterization of structure and antioxidant activity of polysaccharides from sesame seed hull.

[This corrects the article DOI: 10.3389/fnut.2022.928972.].

Characterization of Structure and Antioxidant Activity of Polysaccharides From Sesame Seed Hull.

Sesame seed hull is the major by-product of sesame seed processing and is rich in polysaccharides. In this work, sesame hull polysaccharides (SHP) were extracted by ultrasound-assisted alkali extraction methods with a yield of 6.49%. Three purified polysaccharide fractions were obtained after decolorization, deproteinization, and column chromatography. Then, their main composition and antioxidant activity were investigated. The dominant fraction was SHP-2 with a yield of 3.78%. It was composed of galacturonic acid (51.3%), glucuronic acid (13.8%), rhamnose (8.9%), glucose (8.4%), and others. The linkage types of SHP-2 have the α-D-GalpA-(1,4)-linked, α-D-GlcpA-(1,2)-linked, ß-T-D-Rhap-linked, ß-D-Glcp-(1,6)-linked, ß-T-D-Galp-linked, α-L-Xylp-(1,4)-linked, α-L-Araf-(1,3,5)-linked, and ß-D-Manp-(1,4)-linked. This study might provide some useful basic data for developing applications for sesame seed hull polysaccharides in the food and pharmaceutical industries.

Supplementation with Tetrahydrocurcumin Enhances the Therapeutic Effects of Dexamethasone in a Murine Model of Allergic Asthma.

BACKGROUND: Tetrahydrocurcumin (THC) is the major active metabolite of curcumin, which is a dietary factor derived from Curcuma species. Our previous study demonstrated a significant beneficial effect of THC in mice with allergic asthma. Glucocorticosteroids (GCs) are commonly used drugs in asthma. Whether THC supplementation could promote the beneficial effects of GC therapy on asthma has not yet been reported. The current study aimed to investigate the combined efficacy of GC and THC treatment in a mouse model of allergic asthma. METHODS: BALB/c mice were randomly divided into 5 groups: the control group, ovalbumin (OVA)-induced group, and OVA-induced mice treated with dietary THC only, intraperitoneal injection of dexamethasone (DEX) only, or THC combined with DEX. The nasal symptoms, histopathological alterations of lung tissues, lung cytokine production, and Th cell subsets were assessed. RESULTS: THC or DEX had beneficial effects on nasal symptoms and pathological lung changes, and the therapeutic effects between THC and DEX treatment were comparable. Importantly, compared to the monotherapy groups (THC or DEX only), the combination of THC and DEX showed a significantly reduced nasal rubbing frequency, lower mucus hyperproduction, lower Th2 and Th17 cell numbers as well as lower related cytokine levels (IL-4, IL-5, and IL-17A). CONCLUSIONS: Supplementation with THC can enhance the therapeutic effects of DEX to alleviate airway symptoms, lung inflammation, and the Th2 response. Our findings suggest that dietary administration of THC could act as an add-on therapy for asthma treated with GCs.

Plasma membrane depolarization and Na,K-ATPase impairment induced by mitochondrial toxins augment leukemia cell apoptosis via a novel mitochondrial amplification mechanism.

Na,K-ATPase is a ubiquitous transmembrane protein that regulates and maintains the intracellular Na(+) and K(+) gradient necessary for cell homeostasis. Recently, the importance of this pump in external stimuli-induced leukemia cell apoptosis has been increasingly appreciated, however, the exact role of Na,K-ATPase in mitochondrial apoptotic pathway still remains little understood. In this study, we found mitochondrial toxin rotenone caused a rapid mitochondrial membrane potential (MMP) collapse in Jurkat cells followed by plasma membrane depolarization (PMP). Similar results were also obtained in human U937 cells and non-cancerous mouse primary T cells. Rotenone-induced PMP depolarization occurred before apoptosis and well correlated with Na,K-ATPase impairment. To understand the mechanisms, Jurkat cells with mtDNA depletion and catalase overexpression were used. The results demonstrated that both PMP depolarization and Na,K-ATPase impairment induced by rotenone were regulated by mitochondrial H(2)O(2) and Bcl-2. Finally, Na,K-ATPase suppression by ouabain greatly accelerated and enhanced mitochondrial toxins-induced cells apoptosis in Jurkat, U937 and primary T cells. In sum, by using leukemia cells and mouse primary T cells, we confirmed that mitochondria-to-Na,K-ATPase and PMP depolarization might represent a novel mechanism for mitochondria to amplify death signals in the initiation stage of cells apoptosis induced by mitochondrial toxins.