Pomelo peel oil alleviates cerebral NLRP3 inflammasome activation in a cardiopulmonary resuscitation rat model.

The NLR family pyrin domain-containing 3 (NLRP3) inflammasome, which is composed of NLRP3, apoptosis-associated speck-like protein containing a CARD (ASC) and pro-caspase-1 protein complexes, is activated by the reactive oxygen species (ROS) that are associated with ischemia-reperfusion (I/R) and are involved in brain damage. Pomelo peel oil (PPO) exhibits antioxidant activity. However, it is unclear whether PPO is able to attenuate NLRP3 inflammasome-induced inflammation and pyroptosis. Healthy male Sprague-Dawley rats were subjected to 7 min of cardiac arrest via trans-esophageal electrical stimulation, followed by cardiopulmonary resuscitation (CPR). The rats were then treated with PPO prior to reperfusion for 24 h. Hematoxylin and eosin staining was used to evaluate brain tissue and cell damage. In the brain tissues, reactive oxygen species (ROS) were assayed, immunofluorescence was used to analyze the expression of NLRP3 and western blotting was performed to determine the expression levels of neuroenolase (NSE), NF-κB, interleukin-1ß (IL-1ß), gasdermin D (GSDMD) and the NLRP3 inflammasome. Treatment of the rats with PPO significantly decreased the pathological damage of the brain tissue and reduced the expression of NSE, production of ROS and secretion of NF-κB, NLRP3, IL-1ß and GSDMD. In conclusion, these results demonstrate the ability of PPO to protect the brain against I/R injury in rats after CPR by a mechanism involving inhibition of the inflammation and pyroptosis mediated by NLRP3 inflammasome activation.

Pomelo Peel Volatile Oil Alleviates Neuroinflammation on Focal Cerebral Ischemia Reperfusion Injury Rats via Inhibiting TLR4/NF-κB Signaling Pathway.

BACKGROUND: Restoration of blood flow during ischemic stroke leads to Cerebral Ischemia- Reperfusion Injury (CIRI) by activating neuroinflammatory cascades. Pomelo Peel Volatile Oil (PPVO) extracted from Citrus maxima (Burm.) from the genus Rutaceae, comprises some antiinflammatory ingredients, such as limonene and ß-myrcene. OBJECTIVE: The present study aimed to investigate the potential effect of PPVO on alleviating CIRI related to the Toll-like receptor 4/nuclear factor-kappa B (TLR4/NF-κB) pathway. METHODS: Transient middle cerebral artery occlusion/reperfusion (tMCAO/R) was performed on 65 rats, which were then distributed into five groups (n = 13/group) depending on the intervention they received: Normal Saline (NS) group, normal Glycerin (GL) group, low-dose PPVO (LP, 10mg/kg) group, high-dose PPVO (HP, 30 mg/kg) group, and Sham-operated (SH) group. Neurological Deficit Scores (NDSs) and histological changes were evaluated. Infarct volumes were measured by 2,3,5- Triphenyltetrazolium Chloride (TTC) staining. The expression of TLR4 and neutrophil infiltration were detected by Immunofluorescence (IF) staining. Moreover, the downstream molecules of the TLR4/NF-κB signaling pathway, such as IL-6, IL-1ß, TNF-α, p-IκB/IκB, and p-NF-κB p65/NF-κB p65 were analyzed by Western Blot (WB). RESULTS AND DISCUSSION: The results showed that PPVO (30 mg/kg) significantly decreased infarct volumes, improved neurological deficits and pathologic changes, inhibited TLR4/NF-κB signaling pathway suppressed neutrophil infiltration, and suppressed pro-inflammatory cytokine release. CONCLUSION: It can be concluded that PPVO may alleviate neuroinflammation and protect against CIRI via inhibiting the TLR4/NF-κB signaling pathway.

Inhibition of extracellular signal-regulated kinase/calpain-2 pathway reduces neuroinflammation and necroptosis after cerebral ischemia-reperfusion injury in a rat model of cardiac arrest.

BACKGROUND: Cerebral ischemia-reperfusion injury (CIRI) is the leading cause of poor neurological prognosis after cardiopulmonary resuscitation (CPR). We previously reported that the extracellular signal-regulated kinase (ERK) activation mediates CIRI. Here, we explored the potential ERK/calpain-2 pathway role in CIRI using a rat model of cardiac arrest (CA). METHODS: Adult male Sprague-Dawley rats suffered from CA/CPR-induced CIRI, received saline, DMSO, PD98059 (ERK1/2 inhibitor, 0.3 mg/kg), or MDL28170 (calpain inhibitor, 3.0 mg/kg) after spontaneous circulation recovery. The survival rate and the neurological deficit score (NDS) were utilized to assess the brain function. Hematoxylin stain, Nissl staining, and transmission electron microscopy were used to evaluate the neuron injury. The expression levels of p-ERK, ERK, calpain-2, neuroinflammation-related markers (GFAP, Iba1, IL-1ß, TNF-α), and necroptosis proteins (TNFR1, RIPK1, RIPK3, p-MLKL, and MLKL) in the brain tissues were determined by western blotting and immunohistochemistry. Fluorescent multiplex immunohistochemistry was used to analyze the p-ERK, calpain-2, and RIPK3 co-expression in neurons, and RIPK3 expression levels in microglia or astrocytes. RESULTS: At 24 h after CA/CPR, the rats in the saline-treated and DMSO groups presented with injury tissue morphology, low NDS, ERK/calpain-2 pathway activation, and inflammatory cytokine and necroptosis protein over-expression in the brain tissue. After PD98059 and MDL28170 treatment, the brain function was improved, while inflammatory response and necroptosis were suppressed by ERK/calpain-2 pathway inhibition. CONCLUSION: Inflammation activation and necroptosis involved in CA/CPR-induced CIRI were regulated by the ERK/calpain-2 signaling pathway. Inhibition of that pathway can reduce neuroinflammation and necroptosis after CIRI in the CA model rats.

Influence of Y3+, Bi3+ content on photoluminescence of YVO4:Dy3+ phosphor induced by ultraviolet excitation.

YxVO4: 0.01Dy3+ and Y0.99-x V04: 0.01Dy3+, xBi3+ phosphors were synthesized by chemical coprecipitation method. Their crystal structure, micromorphology and photoluminescence (PL) properties were investigated by X-ray diffraction (XRD), scan electron microscopy (SEM) and spectrofluorometer. YxVO4: 0.01Dy3+ and Y0.99--xVO4: 0.01Dy3+, xBi3+ phosphors have a broad excitation band from about 250 to 350 nm including a strongest peak at about 310 nm. Under its excitation, the emission spectra exhibits two sharp peaks, one of which centered at about 483 nm for 4F9/2-->6H15/2 transition of Dy3+ and the other at about 574 nm due to the 4F9/2-->6 H13/2 transition of Dy+. For YxVO4: 0.01Dy3+, (x = 0.94, 0.97, 0.99, 1.01, 1.03) phosphor, with increasing value of x, the body color of phosphor changes from yellow to white and the strongest peak in the excitation spectra shifts a little to shorter wavelength. It is detrimental to luminous intensity when Y3+ content deviates stoichiometric ratio. For Y0.99--x VO4: 0.01Dy3+, xBi3+ (x = 0.01, 0.05, 0.1, 0.15, 0.2, 0.25) phosphor, the samples have extraneous bismuth vanadium oxide phase except for the major tetragonal zircon structure when x > or = 0.20. With increasing value of x, the band edge in the excitation spectra shifts to longer wavelength, the excitation intensity and luminous intensity increase early and decrease late. When the value of x is 0.01, the intensities increase evidently. In addition, the influence of Y3+ or Bi3+ on the color temperature of emission and micromorphology of YVO4:Dy3+ is slight.

A novel thiophene-fused polycyclic aromatic with a tetracene core: synthesis, characterization, optical and electrochemical properties.

FeCl3-mediated oxidative cyclization was successfully used to construct an extended thiophene-pendant pyrene skeleton and synthesize a novel thiophene-fused polycyclic aromatic (THTP-C) with a tetracene core. The identity of the compound was confirmed by ¹H-NMR, ¹³C-NMR, MS, and elemental analysis. Meanwhile, a single crystal of THTP-C was obtained and analyzed by X-ray single-crystal diffraction. THTP-C has a "saddle" shaped π-conjugated 1-D supramolecular structure, and favors highly ordered self-assembly by π-π interactions as evidenced by its concentration-dependent ¹H-NMR spectra in solution. The optical properties of THTP-C were investigated by ultraviolet-visible (UV-Vis) and photoluminescence (PL) spectroscopy and its electrochemical properties were investigated by cyclic voltammetry (CV). The relatively large band gap (2.86 eV), low E(HOMO) level (-5.64 eV) and intermolecular π-π interactions imply that THTP-C has a high stability against photo-degradation and oxidation, and may be a promising candidate for stable hole-transporting materials.

[A study on preparation and characteristic of RuO2/TiO2 coupled photocatalyst].

RuO2/TiQ2 coupled photocatalyst was prepared by sol-gel-dipping method. Being a model reaction, the photocatalytic degradation of direct fast black G was investigated in RuO2/TiO2 powder suspension irradiated by UV-lamp. The results showed that the addition of RuO2 to TiO2 greatly enhanced its photocatalytic activity, and the optimum dipped content of RuO2 was 0.16%, the optimum value of the calcinations temperature and the addition of RuO2/TiO2 powder were 500 degrees C and 5.00 g x L(-1), respectively. The photocatalytic degradation of direct fast black G was experimentally demonstrated to follow the Langmuir-Hinshelwood kinetic model, and the adsorption constant (14.22 L x mmol(-1)) and the reaction rate constant [4.94 x 10(-3) mmol(L x min)(-1)] were determined, respectively.