Hollow polyester/kapok/hollow polyester fiber-based needle punched nonwoven composite materials for rapid and efficient oil sorption.

Nowadays oil pollution poses a serious threat to the environment and people's daily life. As reusable and environmentally friendly materials, fiber-based oil sorption materials can effectively alleviate this phenomenon. However, maintaining a high sorption rate along with improved mechanical properties remains a challenge for oil sorption materials. Herein, we report a novel hollow PET/kapok/hollow PET nonwoven with high porosity and oil retention, outstanding cyclic oil sorption rate and improved mechanical performance using kapok as the oil preserver and hollow PET as the conductor and structure enhancer. Benefiting from the three-layer composite structure fabricated by carding and needle punching reinforcement, the resulting oil sorption materials, with kapok proportion more than or equal to 60%, exhibited high oil sorption rate and oil sorption speed. The materials of 20HP/60K/20HP component content present a high initial oil sorption rate of 28.22 g g-1, a maximum oil sorption rate of 31.17 g g-1 and a sorption rate constant of the Quasi second-order kinetic equation of 0.067 in plant oil. On the other hand, when the proportion of kapok fiber in the material was below 60%, due to the introduction of hollow PET, the mechanical properties were significantly boosted, and its oil retention and reusability were distinguished, with a reuse rate stabilizing at a relatively high level (>93%) in plant oil after undergoing three oil sorption cycles. The successful fabrication of hollow PET/kapok/hollow PET nonwovens could provide a new approach for the design and development of oil sorption materials.

Neuroprotective Effects of B-Type Cinnamon Procyanidin Oligomers on MPP+-Induced Apoptosis in a Cell Culture Model of Parkinson's Disease.

Cinnamon procyanidin oligomers (CPOs) are water-soluble components extracted from cinnamon. This study aims to explore the neuroprotection of B-type CPO (CPO-B) against 1-methyl-4-phenylpyridinium (MPP+)-mediated cytotoxicity and the molecular mechanisms underlying its protection. The results demonstrated that CPO-B showed protection by increasing cell viability, attenuating an intracellular level of reactive oxygen species, downregulating cleaved caspase-3 expression, and upregulating the Bcl-2/Bax ratio. Moreover, CPO-B completely blocked the dephosphorylation of extracellular, signal-regulated kinase 1 and 2 (Erk1/2) caused by MPP+. Treatment with an Erk1/2 inhibitor, SCH772984, significantly abolished the neuroprotection of CPO-B against MPP+. Taken together, we demonstrate that CPO-B from cinnamon bark provided protection against MPP+ in cultured SH-SY5Y cells, and the potential mechanisms may be attributed to its ability to modulate the dysregulation between pro-apoptotic and anti-apoptotic proteins through the Erk1/2 signaling pathway. Our findings suggest that the addition of cinnamon to food or supplements might benefit patients with PD.

A-Type Cinnamon Procyanidin Oligomers Protect Against 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine-Induced Neurotoxicity in Mice Through Inhibiting the P38 Mitogen-Activated Protein Kinase/P53/BCL-2 Associated X Protein Signaling Pathway.

BACKGROUND: Parkinson's disease (PD) is a common neurodegenerative disorder. Cinnamon procyanidin oligomers (CPOs) are flavonoids with many claimed health benefits. OBJECTIVE: This study aimed to elucidate the neuroprotection of A-type CPOs (CPO-A) and the underlying mechanisms in cultured cell and animal models of PD. METHODS: Thirty male mice (C57BL/6, 9-wk old) were assigned to 3 groups (n = 10), and were given daily gavage of saline [control and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) groups] or CPO-A (150 mg/kg, CPO-A group) during days 1-15 and daily intraperitoneal injections of saline (control group) or MPTP (20 mg/kg; MPTP and MPTP + CPO-A groups) during days 11-15. After the motor behavior test, all mice were killed on day 16 to collect the substantia nigra (SN) for assaying the neuroprotective effects of CPO-A. SH-SY5Y cells were treated with 12.5 µM CPO-A for 2 h or 3 activators of stress-related kinases (5-25 µM) for 12-48 h followed by 1 mM 1-methyl-4-phenylpyridinium (MPP+) for assays of viability, morphology, and stress status. RESULTS: Compared with the control, the MPTP treatment decreased (P < 0.05) locomotor activity by 21%, and tyrosine hydroxylase (TH) positive neurons by 55% and Th mRNA concentration by 51% in the SN. The CPO-A treatment attenuated or restored (P < 0.05) these changes and inhibited (P < 0.05) the MPTP-induced activation of P38 mitogen-activated protein kinase (P38MAPK) and P53, along with the downstream expression of BCL-2 associated X protein (BAX) in the SN. In SH-SY5Y cells, the CPO-A treatment blocked (P < 0.01) the MPP+-induced accumulation of intracellular reactive oxygen species and neurotoxicity. However, this protection was abolished (P < 0.05) by activators of the P38MAPK/P53/BAX pathway. CONCLUSION: CPO-A protected against MPP+-induced cytotoxicity in SH-SY5Y cells and MPTP-induced neurotoxicity in mice by regulating the P38MAPK/P53/BAX signaling. Our findings reveal a novel role and mechanism of a food flavonoid CPO-A in preventing neurodegeneration.