ABSTRACT
Although gelatin has good characteristics in preparing soft capsules, its noticeable shortcomings force researchers to further develop substitutes for gelatin soft capsules. In this paper, sodium alginate (SA), carboxymethyl starch (CMS) and κ-carrageenan (κ-C) were used as matrix materials, and the formula of the co-blended solutions was screened through rheological method. In addition, films of the different blends were characterized by thermogravimetry analysis, SEM, FTIR, X-ray, water contact angle and mechanical properties. The results showed that κ-C had strong interaction with CMS and SA, and the mechanical properties of capsule shell were greatly improved by the addition of κ-C. When the ratio of CMS/SA/κ-C was 2:0.5:1.5, the microstructure of the films was more dense and uniform. In addition, this formula had the best mechanical properties and adhesion properties, and was more suitable for the production of soft capsules. Finally, a novel plant soft capsule was successfully prepared by dropping method, and its appearance and rupture properties met the requirements of enteric soft capsules. In simulated intestinal fluid, the soft capsules were almost completely degraded within 15 min, and they were superior to the gelatin soft capsules. Therefore, this study provides an alternative formula for preparing enteric soft capsules.
Subject(s)
Gelatin , Starch , Carrageenan/chemistry , Capsules/chemistry , Gelatin/chemistry , Starch/chemistryABSTRACT
AIM: Multiple sclerosis (MS) is a neurological autoimmune disorder characterized by mistaken attacks of inflammatory cells against the central nervous system (CNS), resulting in demyelination and axonal damage. Kv1.3 channel blockers can inhibit T-cell activation and have been designed for MS therapy. However, little is known about the effects of Kv1.3 blockers on protecting myelin sheaths/axons in MS. This study aimed at investigating the neuroprotection efficacy of a selective Kv1.3 channel blocker ImKTx88 (ImK) in MS animal model. METHODS: Experimental autoimmune encephalomyelitis (EAE) rat model was established. The neuroprotective effect of ImK was assessed by immunohistochemistry and transmission electron microscopy (TEM). In addition, the antiinflammatory effect of ImK by suppressing T-cell activation was assessed by flow cytometry and ELISA in vitro. RESULTS: Our results demonstrated that ImK administration ameliorated EAE clinical severity. Moreover, ImK increased oligodendrocytes survival, preserved axons, and myelin integrity and reduced the infiltration of activated T cells into the CNS. This protective effect of the peptide may be related to its suppression of autoantigen-specific T-cell activation via calcium influx inhibition. CONCLUSION: ImK prevents neurological damage by suppressing T-cell activation, suggesting the applicability of this peptide in MS therapy.
