The thermal mechanical properties and morphological changes of modified poly(lactic acid) (PLA) and polycarbonate (PC) polymer blends based on the equal weight fraction of each component were investigated. Several blend samples were prepared by melt processing with a twin screw extruder using both poly(butylene succinate-co-lactate) (PBSL) and epoxy (EP) as compatibilizers for the PLA/PC binary system. Differential scanning calorimetry (DSC) of PLA/PBSL and PC/PBSL binary blends showed that individual components were immiscible. Scanning electron microscopy (SEM) analysis of these blends revealed the domain size of PBSL was $ 0.5-1 lm in PLA/PBSL blend, and reduced to around 0.1 lm in PC/PBSL blend. The notched Izod impact strength (IS) of PLA/PC/PBSL ternary blends increased with PBSL content up to 10 phr PBSL due to enhanced interfacial interaction and proper domain size of the dispersed phase on the basis of DMA, DSC, and SEM analysis. The heat deflection temperature (HDT) showed a maximum at 5 phr PBSL, and it dropped with increasing PBSL content which is a ductile polymer. However, the HDT of PLA/PC/EP ternary blends increased considerably with 10 phr EP due to rigid interphase formation, and it increased further with 1 phr quaternary amine catalyst, however, the IS dropped nearly the same as that of unmodified PLA/PC blend. To take advantage of the two compatibilizers, PBSL and EP were added to the PLA/PC blend at 10 phr each plus 1 phr catalyst and both IS and HDT were improved significantly over unmodified PLA/PC pair.

Background Glossogyne tenuifolia (GT) is a traditional herbal tea in Penghu Island, Taiwan. Its extract is traditionally been used as an antipyretic, hepatoprotective and anti-inflammatory remedy in folk medicine among local residents. The present study investigated whether GT could improve streptozotocin-induced acute liver injury of type 2 diabetes mellitus. Methods Male Wistar rats aged eight weeks were induced to be hyperglycemic by the subcutaneous injection of streptozotocin-nicotinamide (STZ-NA) and a combination of a high-fat diet (HFD) (N group). The animals were given GT extracts at a low dose (50 mg/kg) (L group) or a high dose (150 mg/kg) (H group) or an anti-diabetic drug (acarbose) (P group) in drinking water for 4 weeks. Results The results revealed that STZ-NA increased hepatomegaly, hepatocyte cross-sectional area, hypertrophy-related pathways (IL6/STAT3-MEK5-ERK5, NFATc3, p38 and JNK MAPK), proapoptotic molecules (cytochrome C, cleaved caspase-3), and fibrosis-related pathways (FGF-2, pERK1/2). These pathway components were then expressed at lower levels in the L and H group when compared with the N group. The liver-protective effect of GT in STZ-NA-induced diabetic rats with hyperlipidemia was through an enhancement in the activation of the compensatory PI3K-Akt and Bcl2 survival-related pathway. Conclusion The results demonstrate that the hot water extracts of GT efficiently ameliorates the STZ-NA-induced diabetes associated liver damage in rat models.

Obesity is generally associated with low-grade chronic inflammation that involves the recruitment of macrophages and other inflammation factors to the adipocytes of obese individuals. Tumor necrosis factor-alpha (TNF-α), a cytokine associated with systemic inflammation, is elevated in conditions of obesity. TNF-α is an important factor that plays an important role in skeletal muscle wasting. Apoptosis of myonuclei contributes to the loss of muscle mass and therefore plays an important role in skeletal muscle atrophy. In mouse models that were fed a high fat diet (HFD), a lipolysis-stimulating peptide-VHVV (purified from hydrolysate resulting from flavourzyme treatment of soy protein) was found to reduce HFD-related apoptotic effects in mice skeletal muscle and potentially control atrophy. HFD fed mice had heavier body weight than those fed with normal chow, and VHVV administration restricted lipid accumulation in muscle tissues of mice fed with HFD but increased nutrient uptake. Moreover, specific concentrations of VHVV regulated TNF-α expression that was elevated by HFD, suppressed apoptosis-related proteins and regulated the proteins of lipid metabolism.

BackgroundA potato protein hydrolysate, APPH is a potential anti-obesity diet ingredient. Since, obesity leads to deterioration of liver function and associated liver diseases, in this study the effect of APPH on high fat diet (HFD) associated liver damages was investigated.MethodsSix week old male hamsters were randomly separated to six groups (n = 8) as control, HFD (HFD fed obese), L-APPH (HFD + 15 mg/kg/day of APPH), M-APPH (HFD + 30 mg/kg/day), H-APPH (HFD + 75 mg/kg/day of APPH) and PB (HFD + 500 mg/kg/day of probucol). HFD fed hamsters were administered with APPH 50 days through oral gavage. The animals were euthanized and the number of apoptotic nuclei in liver tissue was determined by TUNEL staining and the extent of interstitial fibrosis was determined by Masson’s trichrome staining. Modulation in the molecular events associated with apoptosis and fibrosis were elucidated from the western blotting analysis of the total protein extracts.ResultsHamsters fed with high fat diet showed symptoms of liver damage as measured from serum markers like alanine aminotransferase and aspartate aminotransferase levels. However a 50 day long supplementation of APPH effectively ameliorated the effects of HFD. HFD also modulated the expression of survival and apoptosis proteins in the hamster liver. Further the HFD groups showed elevated levels of fibrosis markers in liver. The increase in fibrosis and apoptosis was correlated with the increase in the levels of phosphorylated extracellular signal-regulated kinases (pERK1/2) revealing a potential role of ERK in the HFD mediated liver damage. However APPH treatment reduced the effect of HFD on the apoptosis and fibrosis markers considerably and provided hepato-protection.ConclusionAPPH can therefore be considered as an efficient therapeutic agent to ameliorate high fat diet related liver damages.