Stanniocalcin-1 Protected Astrocytes from Hypoxic Damage Through the AMPK Pathway.

Our previous studies revealed that the expression of stanniocalcin-1 (STC1) in astrocytes increased under hypoxic conditions. However, the role of STC1 in hypoxic astrocytes is not well understood. In this work, we first showed the increased expression of STC1 in astrocyte cell line and astrocytes in the brain tissues of mice after exposure to hypoxia. Then, we found that knockdown of STC1 inhibited cell viability and increased apoptosis. These effects were mediated by decreasing the levels of SIRT3, UCP2, and glycolytic genes and increasing the levels of ROS. Further studies suggested that STC1 silencing promoted oxidative stress and suppressed glycolysis by downregulating AMPKα1. Moreover, HIF-1α knockdown in hypoxic astrocytes led to decreased expression of STC1 and AMPKα1, indicating that the expression of STC1 was regulated by HIF-1α. In conclusion, our study showed that HIF-1α-induced STC1 could protect astrocytes from hypoxic damage by regulating glycolysis and redox homeostasis in an AMPKα1-dependent manner.

Targeting mitochondria-associated membranes as a potential therapy against endothelial injury induced by hypoxia.

Mitochondrial dysfunction plays a principal role in hypoxia-induced endothelial injury, which is involved in hypoxic pulmonary hypertension and ischemic cardiovascular diseases. Recent studies have identified mitochondria-associated membranes (MAMs) that modulate mitochondrial function under a variety of pathophysiological conditions such as high-fat diet-mediated insulin resistance, hypoxia reoxygenation-induced myocardial death, and hypoxia-evoked vascular smooth muscle cell proliferation. However, the role of MAMs in hypoxia-induced endothelial injury remains unclear. To explore this further, human umbilical vein endothelial cells and human pulmonary artery endothelial cells were exposed to hypoxia (1% O2 ) for 24 hours. An increase in MAM formation was uncovered by immunoblotting and immunofluorescence. Then, we performed small interfering RNA transfection targeted to MAM constitutive proteins and explored the biological effects. Knockdown of MAM constitutive proteins attenuated hypoxia-induced elevation of mitochondrial Ca2+ and repressed mitochondrial impairment, leading to an increase in mitochondrial membrane potential and ATP production and a decline in reactive oxygen species. Then, we found that MAM disruption mitigated cell apoptosis and promoted cell survival. Next, other protective effects, such as those pertaining to the repression of inflammatory response and the promotion of NO synthesis, were investigated. With the disruption of MAMs under hypoxia, inflammatory molecule expression was repressed, and the eNOS-NO pathway was enhanced. This study demonstrates that the disruption of MAMs might be of therapeutic value for treating endothelial injury under hypoxia, suggesting a novel strategy for preventing hypoxic pulmonary hypertension and ischemic injuries.

Nogo-B Receptor Directs Mitochondria-Associated Membranes to Regulate Vascular Smooth Muscle Cell Proliferation.

Mitochondria-associated membranes (MAM) are a well-recognized contact link between the mitochondria and endoplasmic reticulum that affects mitochondrial biology and vascular smooth muscle cells (VSMCs) proliferation via the regulation of mitochondrial Ca2+(Ca2+m) influx. Nogo-B receptor (NgBR) plays a vital role in proliferation, epithelial-mesenchymal transition, and chemoresistance of some tumors. Recent studies have revealed that downregulation of NgBR, which stimulates the proliferation of VSMCs, but the underlying mechanism remains unclear. Here, we investigated the role of NgBR in MAM and VSMC proliferation. We analyzed the expression of NgBR in pulmonary arteries using a rat model of hypoxic pulmonary hypertension (HPH), in which rats were subjected to normoxic recovery after hypoxia. VSMCs exposed to hypoxia and renormoxia were used to assess the alterations in NgBR expression in vitro. The effect of NgBR downregulation and overexpression on VSMC proliferation was explored. The results revealed that NgBR expression was negatively related with VSMCs proliferation. Then, MAM formation and the phosphorylation of inositol 1,4,5-trisphosphate receptor type 3 (IP3R3) was detected. We found that knockdown of NgBR resulted in MAM disruption and augmented the phosphorylation of IP3R3 through pAkt, accompanied by mitochondrial dysfunction including decreased Ca2+m, respiration and mitochondrial superoxide, increased mitochondrial membrane potential and HIF-1α nuclear localization, which were determined by confocal microscopy and Seahorse XF-96 analyzer. By contrast, NgBR overexpression attenuated IP3R3 phosphorylation and HIF-1α nuclear localization under hypoxia. These results reveal that dysregulation of NgBR promotes VSMC proliferation via MAM disruption and increased IP3R3 phosphorylation, which contribute to the decrease of Ca2+m and mitochondrial impairment.

Egg yolk phospholipids: a functional food material to generate deep-fat frying odorants.

BACKGROUND: Phospholipids are an important precursor for the generation of carbonyl compounds that play a significant role in the characteristic aroma of deep-fat fried foods. RESULTS: Phospholipids extracted from hen egg yolks were added into sunflower oil (2.0 g kg-1 ) and heated with or without chicken meat at 160 °C for 10 min, and then dynamic headspace extraction and gas chromatography-mass spectrometry were used to extract and analyse the volatiles. The results showed that the characteristic deep-fat frying odorants, such as (E,E)-2,4-decadienal and (E,Z)-2,4-decadienal, as well as 1-octen-3-one, (E)-2-nonenal, octanal, methional, dimethyl disulfide and alkylpyrazines, had increased by 3-65 times in the sunflower oil with added phospholipids, and increased up to six times in chicken meat that had been treated with phospholipids prior to heating. CONCLUSION: There is potential for the food industry to use low levels of phospholipids, particularly egg yolk phospholipids, to increase deep-fat frying odorants in a wide range of deep-fried products. © 2019 Society of Chemical Industry.

Treatments of tilapia (Oreochromis niloticus) using nitric oxide for quality improvement: Establishing a potential method for large-scale processing of farmed fish.

BACKGROUND: To find a succedaneum of present methods for slaughtering tilapia, we have demonstrated the influence of nitric oxide (NO) (saturated NO solution) through euthanasia before slaughter on the animal welfare and muscle color of tilapia. The results suggested that NO euthanasia significantly improved the animal welfare and muscle color. Besides, the investigation of NO postmortem treatment on the muscle color and color stability of tilapia fillets suggested that NO postmortem treatment not only improved the muscle color and color stability but also prolonged the shelf-life of tilapia fillets during the refrigerated storage. OBJECTIVE: To further investigate the effect of NO euthanasia on the quality of tilapia fillets and to estimate the safety of NO treatments (NO euthanasia and NO postmortem treatment) for the application of NO treatments in industrial manufacturing of tilapia and possibly of other fish species. METHODS: NO euthanasia was adopted in this study following a simulated fish processing line. HbNO and MbNO values were measured to clarify the mechanism and process of NO euthanasia. The blood parameters, muscle pH, rigor index, drip loss and total volatile basic nitrogen (TVB-N) values were measured to evaluate the quality of the fillets obtained from NO euthanized tilapia. Besides, the nitrate (NO3-) levels in the muscles after the refrigerated storage were detected to estimate the food safety of both NO euthanasia and NO postmortem treatment. RESULTS: Fillets obtained from the tilapia euthanized by NO showed a later reduction of muscle pH, a later onset of rigor mortis postmortem and less drip loss during the refrigerated storage than control. NO euthanasia caused less TVB-N than control and prolonged the shelf life of tilapia fillets. Moreover, the NO3- levels in the muscles of both NO euthanasia and NO postmortem treatment after the refrigerated storage were below the maximum permitted limit. CONCLUSION: Both the NO euthanasia and NO postmortem treatment are suitable for improving the quality of tilapia fillets and reducing the food safety threats, which may be valuable for industrial manufacturing of tilapia and may be applicable for other fish species.

Influence of postmortem treatment with nitric oxide on the muscle color and color stability of tilapia (Oreochromis niloticus) fillets.

BACKGROUND: Nitric oxide (NO) has been recognized as pivotal for color and color stability of meat products and has an evident effect on inhibiting microbial growth in processed meat. The use of indirect NO (nitrate/nitrite) in industrial meat curing has potential deleterious effects and great concerns have been expressed over residual nitrite in meat after curing. To find a succedaneum, we have demonstrated the influence of direct NO (saturated NO solution) through euthanasia before slaughter on the fillets color of tilapia and the results suggested that direct NO treatment prior to slaughter is a good procedure to improve the color of tilapia fillets. OBJECTIVE: To further investigate the effect of direct NO on the muscle color and shelf-life of fillets from tilapia, this study was conducted to investigate the muscle color and color stability of tilapia fillets postmortem treated with saturated NO solution and their shelf-life during refrigerated storage. METHODS: Tilapia fillets were immersed in a saturated NO solution for 13 min, vacuum-packed and stored at refrigerated temperature for 15 days. Visual observations, color values and absorption maxima were used to evaluate the muscle color and color stability of tilapia fillets. Total volatile basic nitrogen (TVB-N) values were used to evaluate the shelf-life of tilapia fillets during refrigerated storage. RESULTS: By visual observation, NO treated tilapia fillets showed a brighter red color as compered to control samples after NO-treatment and during the whole storage. The redness (a*) values of NO treated tilapia fillets were significantly increased (P < 0.05) after NO-treatment, continuously increased (P < 0.05) during the earlier 9 days of the storage and remained roughly unchanged during the rest days of the storage. While the a* values of control samples decreased progressively during the storage. NO-treatment effectively improved the muscle color and color stability of tilapia fillets. The peak wavelengths of extract from the muscles of NO treated tilapia fillets increased from 418 nm to 421 nm at 15 d of the storage, while that of control decreased from 418 nm to 410 nm, indicated that color improvement in NO-treated tilapia fillets is mainly due to the formation of MbNO. Moreover, NO-treatment resulted in less TVB-N values than control (16.06 and 21.93 mg of N/100 g at the end of the storage, respectively), prolonging the shelf-life of tilapia fillets. CONCLUSION: The results suggested that postmortem treatment with NO is a good procedure not only for improving the muscle color and color stability but also for prolonging the shelf-life of tilapia fillets during the storage, which is valuable for industrial manufacturing of tilapia and possibly for other fish species.

Critical effects of epigenetic regulation in pulmonary arterial hypertension.

Pulmonary arterial hypertension (PAH) is characterized by persistent pulmonary vasoconstriction and pulmonary vascular remodeling. The pathogenic mechanisms of PAH remain to be fully clarified and measures of effective prevention are lacking. Recent studies; however, have indicated that epigenetic processes may exert pivotal influences on PAH pathogenesis. In this review, we summarize the latest research findings regarding epigenetic regulation in PAH, focusing on the roles of non-coding RNAs, histone modifications, ATP-dependent chromatin remodeling and DNA methylation, and discuss the potential of epigenetic-based therapies for PAH.

Endothelial MRTF-A mediates angiotensin II induced cardiac hypertrophy.

Angiotensin II (Ang II) stimulates endothelin (ET-1) transcription, which contributes to cardiac hypertrophy and fibrosis. We have previously reported that myocardin related transcription factor A (MRTF-A) is indispensable for ET-1 transcription in vascular endothelial cells under hypoxic conditions, indicating that MRTF-A might mediate Ang II-induced pathological hypertrophy. Here we report that Ang II augmented the expression of MRTF-A in cultured endothelial cells and in the lungs of mice with cardiac hypertrophy. Over-expression of MRTF-A enhanced, whereas depletion of MRTF-A attenuated, transcriptional activation of ET-1 gene by Ang II. MRTF-A deficiency ameliorated Ang II induced cardiac hypertrophy and fibrosis in mice paralleling diminished synthesis and release of ET-1. Mechanistically, MRTF-A was recruited to the ET-1 promoter by c-Jun/c-Fos (AP-1) in response to Ang II treatment. Once bound, MRTF-A altered the chromatin structure by modulating histone acetylation and H3K4 methylation on the ET-1 promoter. More importantly, mice with endothelial-specific MRTF-A silencing by lentiviral particles phenocopied mice with systemic MRTF-A deletion in terms of Ang II-induced pathological hypertrophy. In conclusion, we data have unveiled a MRTF-A-containing complex that links ET-1 transactivation in endothelial cells to cardiac hypertrophy and fibrosis by Ang II.

Proinflammatory stimuli engage Brahma related gene 1 and Brahma in endothelial injury.

RATIONALE: Endothelial dysfunction inflicted by inflammation is found in a host of cardiovascular pathologies. One hallmark event in this process is the aggregation and adhesion of leukocyte to the vessel wall mediated by the upregulation of adhesion molecules (CAM) in endothelial cells at the transcriptional level. The epigenetic modulator(s) of CAM transactivation and its underlying pathophysiological relevance remain poorly defined. OBJECTIVE: Our goal was to determine the involvement of Brahma related gene 1 (Brg1) and Brahma (Brm) in CAM transactivation and its relevance in the pathogenesis of atherosclerosis. METHODS AND RESULTS: In the present study, we report that proinflammatory stimuli augmented the expression of Brg1 and Brm in vitro in cultured endothelial cells and in vivo in arteries isolated from rodents. Overexpression of Brg1 and Brm promoted while knockdown of Brg1 and Brm abrogated transactivation of adhesion molecules and leukocyte adhesion induced by inflammatory signals. Brg1 and Brm interacted with and were recruited to the CAM promoters by nuclear factor κB/p65. Conversely, depletion of Brg1 and Brm disrupted the kinetics of p65 binding on CAM promoters and crippled CAM activation. Silencing of Brg1 and Brm also altered key epigenetic changes associated with CAM transactivation. Of intrigue, 17ß-estradiol antagonized both the expression and activity of Brg1/Brm. Most importantly, endothelial-targeted elimination of Brg1/Brm conferred atheroprotective effects to Apoe(-/-) mice on a Western diet. CONCLUSIONS: Our data suggest that Brg1 and Brm integrate various proinflammatory cues into CAM transactivation and endothelial malfunction and, as such, may serve as potential therapeutic targets in treating inflammation-related cardiovascular diseases.

Megakaryocytic leukemia 1 (MKL1) ties the epigenetic machinery to hypoxia-induced transactivation of endothelin-1.

Increased synthesis of endothelin-1 (ET-1) by human vascular endothelial cells (HVECs) in response to hypoxia underscores persistent vasoconstriction observed in patients with pulmonary hypertension. The molecular mechanism whereby hypoxia stimulates ET-1 gene transcription is not well understood. Here we report that megakaryocytic leukemia 1 (MKL1) potentiated hypoxia-induced ET-1 transactivation in HVECs. Disruption of MKL1 activity by either a dominant negative mutant or small interfering RNA mediated knockdown dampened ET-1 synthesis. MKL1 was recruited to the proximal ET-1 promoter region (-81/+150) in HVECs challenged with hypoxic stress by the sequence-specific transcription factor serum response factor (SRF). Depletion of SRF blocked MKL1 recruitment and blunted ET-1 transactivation by hypoxia. Chromatin immunoprecipitation analysis of the ET-1 promoter revealed that MKL1 loss-of-function erased histone modifications consistent with transcriptional activation. In addition, MKL1 was indispensable for the occupancy of Brg1 and Brm, key components of the chromatin remodeling complex, on the ET-1 promoter. Brg1 and Brm modulated ET-1 transactivation by impacting histone modifications. In conclusion, our data have delineated a MKL1-centered complex that links epigenetic maneuverings to ET-1 transactivation in HVECs under hypoxic conditions.

Use of egg yolk phospholipids to improve the thermal-oxidative stability of fatty acids, capsaicinoids and carotenoids in chili oil.

Phospholipids can act as antioxidants in food. In this study, egg yolk phospholipids (EPL) and sunflower oil were utilized in making chili oil, and proton nuclear magnetic resonance spectroscopy was employed to quantify the concentrations of fatty acyl groups, carotenoids, capsaicinoids in chili oil according to their specific signals in the spectra. The results showed that the changes in the concentrations of fatty acyl groups in the control samples were greater than those in the EPL-treated samples at the same frying temperature, while the contents of carotenoids and capsaicinoids were significantly lower than those of the EPL-treated samples when fried at 150 °C (p < 0.05). Two-way ANOVA indicated that frying temperature and EPL treatment, as well as their interaction had significant impacts on the thermal-oxidative stability of chili oil (p < 0.05). The results suggest that EPL may act as antioxidants during frying, and EPL can improve the thermal-oxidative stability of chili oil.

Nitric Oxide Ameliorates the Effects of Hypoxia in Mice by Regulating Oxygen Transport by Hemoglobin.

Xiaoying Zhou, Wenting Su, Quanwei Bao, Yu Cui, Xiaoxu Li, Yidong Yang, Chengzhong Yang, Chengyuan Wang, Li Jiao, Dewei Chen, and Jian Huang. Nitric oxide ameliorates the effects of hypoxia in mice by regulating oxygen transport by hemoglobin. High Alt Med Biol. 00:00-00, 2024.-Hypoxia is a common pathological and physiological phenomenon in ischemia, cancer, and strenuous exercise. Nitric oxide (NO) acts as an endothelium-derived relaxing factor in hypoxic vasodilation and serves as an allosteric regulator of hemoglobin (Hb). However, the ultimate effects of NO on the hematological system in vivo remain unknown, especially in extreme environmental hypoxia. Whether NO regulation of the structure of Hb improves oxygen transport remains unclear. Hence, we examined whether NO altered the oxygen affinity of Hb (Hb-O2 affinity) to protect extremely hypoxic mice. Mice were exposed to severe hypoxia with various concentrations of NO, and the survival time, exercise capacity, and other physical indexes were recorded. The survival time was prolonged in the 5 ppm NO (6.09 ± 1.29 minutes) and 10 ppm NO (6.39 ± 1.58 minutes) groups compared with the 0 ppm group (4.98 ± 1.23 minutes). Hypoxia of the brain was relieved, and the exercise exhaustion time was prolonged when mice inhaled 20 ppm NO (24.70 ± 6.87 minutes vs. 20.23 ± 6.51 minutes). In addition, the differences in arterial oxygen saturation (SO2%) (49.64 ± 7.29% vs. 42.90 ± 4.30%) and arteriovenous SO2% difference (25.14 ± 8.95% vs. 18.10 ± 6.90%) obviously increased. In ex vivo experiments, the oxygen equilibrium curve (OEC) left shifted as P50 decreased from 43.77 ± 2.49 mmHg (0 ppm NO) to 40.97 ± 1.40 mmHg (100 ppm NO) and 38.36 ± 2.78 mmHg (200 ppm NO). Furthermore, the Bohr effect of Hb was enhanced by the introduction of 200 ppm NO (-0.72 ± 0.062 vs.-0.65 ± 0.051), possibly allowing Hb to more easily offload oxygen in tissue at lower pH. The crystal structure reveals a greater distance between Asp94ß-His146ß in nitrosyl -Hb(NO-Hb), NO-HbßCSO93, and S-NitrosoHb(SNO-Hb) compared to tense Hb(T-Hb, 3.7 Å, 4.3 Å, and 5.8 Å respectively, versus 3.5 Å for T-Hb). Moreover, hydrogen bonds were less likely to form, representing a key limitation of relaxed Hb (R-Hb). Upon NO interaction with Hb, hydrogen bonds and salt bridges were less favored, facilitating relaxation. We speculated that NO ameliorated the effects of hypoxia in mice by promoting erythrocyte oxygen loading in the lung and offloading in tissues.

Hypoxia-Induced Myocardial Hypertrophy Companies with Apoptosis Enhancement and p38-MAPK Pathway Activation.

Li, Xiaoxu, Zhijun Pu, Gang Xu, Yidong Yang, Yu Cui, Xiaoying Zhou, Chenyuan Wang, Zhifeng Zhong, Simin Zhou, Jun Yin, Fabo Shan, Chengzhong Yang, Li Jiao, Dewei Chen, and Jian Huang. Hypoxia-induced myocardial hypertrophy companies with apoptosis enhancement and p38-MAPK pathway activation. High Alt Med Biol. 00:00-00, 2024. Background: Right ventricular function and remodeling are closely associated with symptom severity and patient survival in hypoxic pulmonary hypertension. However, the detailed molecular mechanisms underlying hypoxia-induced myocardial hypertrophy remain unclear. Methods: In Sprague-Dawley rats, hemodynamics were assessed under both normoxia and hypobaric hypoxia at intervals of 7 (H7), 14 (H14), and 28 (H28) days. Morphological changes in myocardial tissue were examined using hematoxylin and eosin (HE) staining, while myocardial hypertrophy was evaluated with wheat germ agglutinin (WGA) staining. Apoptosis was determined through TUNEL assays. To further understand the mechanism of myocardial hypertrophy, RNA sequencing was conducted, with findings validated via Western blot analysis. Results: The study demonstrated increased hypoxic pulmonary hypertension and improved right ventricular diastolic and systolic function in the rat models. Significant elevations in pulmonary arterial systolic pressure (PASP), mean pulmonary arterial pressure (mPAP), right ventricular mean pressure (RVMP), and the absolute value of +dp/dtmax were observed in the H14 and H28 groups compared with controls. In addition, right ventricular systolic pressure (RVSP), -dp/dtmax, and the mean dp/dt during isovolumetric relaxation period were notably higher in the H28 group. Heart rate increased in the H14 group, whereas the time constant of right ventricular isovolumic relaxation (tau) was reduced in both H14 and H28 groups. Both the right heart hypertrophy index and the heart weight/body weight ratio (HW/BW) were elevated in the H14 and H28 groups. Myocardial cell cross-sectional area also increased, as shown by HE and WGA staining. Western blot results revealed upregulated HIF-1α levels and enhanced HIF-2α expression in the H7 group. In addition, phosphorylation of p38 and c-fos was augmented in the H28 group. The H28 group showed elevated levels of Cytochrome C (Cyto C), whereas the H14 and H28 groups exhibited increased levels of Cleaved Caspase-3 and the Bax/Bcl-2 ratio. TUNEL analysis revealed a rise in apoptosis with the extension of hypoxia duration in the right ventricle. Conclusions: The study established a link between apoptosis and p38-MAPK pathway activation in hypoxia-induced myocardial hypertrophy, suggesting their significant roles in this pathological process.

SIRT1 links CIITA deacetylation to MHC II activation.

Antigen-dependent stimulation of T cells plays a critical role in adaptive immunity and host defense. Activation of major histocompatibility complex II (MHC II) molecules, dictated by Class II transactivator (CIITA), is considered a pivotal step in this process. The mechanism underlying differential regulation of CIITA activity by the post-translational modification machinery (PTM) and its implications are not clearly appreciated. Here, we report that SIRT1, a type III deacetylase, interacts with and deacetylates CIITA. SIRT1 activation augments MHC II transcription by shielding CIITA from proteasomal degradation and promoting nuclear accumulation and target binding of CIITA. In contrast, depletion of SIRT1 upregulates CIITA acetylation and attenuates its activity. Nicotinamide phosphoribosyltransferase (NAMPT) that synthesizes NAD(+) required for SIRT1 activation exerts similar effects on CIITA activity. Two different types of stress stimuli, hypobaric hypoxia and oxidized low-density lipoprotein (oxLDL), induce the acetylation of CIITA and suppress its activity by inhibiting the SIRT1 expression and activity. Thus, our data link SIRT1-mediated deacetylation of CIITA to MHC II transactivation in macrophages and highlight a novel strategy stress cues may employ to manipulate host adaptive immune system.

Egg yolk phospholipids as an ideal precursor of fatty note odorants for chicken meat and fried foods: A review.

Egg yolk phospholipids (PLs) have been demonstrated to generate large quantities of lipid-derived odorants, especially the fatty note odorants. Recently, egg yolk PLs have been successfully used in chicken meat and fried foods to improve aroma. This review comprehensively summarizes the properties of egg yolk PLs as precursors of fatty note odorants, including their classes, extraction, identification, oxidation, decomposition and odorant formation, applications, considerations and future prospects in the food industry. Most likely, phosphatidylcholine (PC) is the most abundant class in egg yolk PLs, and PC is more efficient than phosphatidylethanolamine in generating fatty note odorants; moreover, the predominant polyunsaturated fatty acid is linoleic acid, and its corresponding predominant hydroperoxide is 9-hydroperoxy-10,12-octadecadienoic acid during autoxidation, which is the precursor of 2,4-decadienals and 2,4-nonadienals, the key fatty note odorants. Therefore, egg yolk PLs could be an ideal precursor of fatty note odorants for chicken meat and fried foods.

Investigation on the changes of carotenoids and capsaicinoids in chili oil at different frying temperature by using 1H NMR.

The color and pungency are important indicators for evaluating the quality of chili oil, which are mainly determined by the carotenoids and capsaicinoids, respectively. In this study, the effect of frying temperature on the changes of carotenoids and capsaicinoids in chili oil was qualitatively and quantitatively analyzed by 1H NMR. The increasing frying temperature caused the thermal degradation of carotenoids to be intensified, and the degradation of red carotenoids was greater than that of yellow carotenoids. After 10 min of frying at 130, 150, 170 and 190 °C, the contents of capsanthin in chili oil were 40.3, 15.4, 9.6 and 6.2 mg/kg, respectively. Meanwhile, the contents of total carotenoids were 63.0, 25.5, 17.7 and 13.3 mg/kg, respectively. The observed change of R/Y values correlated well with the degradation of carotenoids. The contents of capsaicinoids were 14.8, 20.9, 19.4 and 7.4 mg/kg, respectively. The best frying temperature for the extraction of carotenoids was 130 °C, and over 90% of the carotenoids were dissolved in the frying oil at this frying condition. However, capsaicinoids were more stable than carotenoids, and the best frying temperature for capsaicinoids was 150-170 °C with over 90% extraction rate. Therefore, the temperature fried at 130-150 °C was suitable for the quality of chili oil, considering the higher extraction rates of both total carotenoids and capsaicinoids. This study is of great significance for the quality control of chili oil.

The effect of lutein on the oxidation of egg yolk phospholipids in a liposome model.

Egg yolk phospholipids (PLs) extracted by organic solvent are prone to oxidation, while they are quite stable in egg yolk. This study was to verify the decisive role of lutein (naturally present in egg yolk) on the oxidative stability of PLs by constructing liposome. The liposome samples were heated at 100 °C for 10 min, and then the oxidation products of the liposome samples were analyzed by 1H NMR and GC-MS. The results showed that the concentrations of most of the oxidation products in the PLs-liposomes sample were significantly higher than those in the PLs&lutein-liposomes sample. Therefore, lutein could protect egg yolk PLs from oxidation, thus inhibiting the formation of lipid-derived volatile compounds. As those lipid-derived volatile compounds are the key fatty note odorants, this study has confirmed that the removal of lutein is the determining factor in using egg yolk PLs as an ideal precursor of fatty note odorants.

Sinomenine alleviates lipopolysaccharide-induced acute lung injury via a PPARß/δ-dependent mechanism.

Evidence is mounting that sinomenine and peroxisome proliferator-activated receptor ß/δ (PPARß/δ) are effective against lipopolysaccharide (LPS)-induced acute lung injury (ALI) via anti-inflammatory properties. However, it is unknown whether PPARß/δ plays a role in the protective effect of sinomenine on ALI. Here, we initially observed that preemptive administration of sinomenine markedly alleviated lung pathological changes, pulmonary edema and neutrophil infiltration, accompanied by inhibition of the expression of the pro-inflammatory cytokines Tumor necrosis factor-α (TNF-α) and Interleukin-6 (IL-6), which were largely reversed following the addition of a PPARß/δ antagonist. Subsequently, we also noticed that sinomenine upregulated adenosine A2A receptor expression in a PPARß/δ-dependent manner in LPS-stimulated bone marrow-derived macrophages (BMDMs). Further investigation indicated that PPARß/δ directly bound to the functional peroxisome proliferator responsive element (PPRE) in the adenosine A2A receptor gene promoter region to enhance the expression of the adenosine A2A receptor. Sinomenine was identified as a PPARß/δ agonist. It could bind with PPARß/δ, and promote the nuclear translocation and transcriptional activity of PPARß/δ. In addition, combined treatment with sinomenine and an adenosine A2A receptor agonist exhibited synergistic effects and better protective roles than their single use against ALI. Taken together, our results reveal that sinomenine exerts advantageous effects on ALI by activating of PPARß/δ, with the subsequent upregulation of adenosine A2A receptor expression, and provide a novel and potential therapeutic application for ALI.

Use of egg yolk to imitate meat aroma.

Egg yolk contains abundant meat precursors, but its odor is quite different from meat aroma. In this study, the lipids in egg yolk were partly removed by acetone or totally removed by chloroform/methanol, and lutein was removed simultaneously by the solvents. Then, the samples were heated, and the volatiles and aroma profiles were analyzed. The results showed that chicken meat aroma and meat aroma were imitated successfully through the removal of neutral lipids and lutein (acetone-treated) and total lipids and lutein (chloroform/methanol-treated) egg yolk samples, respectively. Finally, additional lutein and tert-butylhydroquinone were employed for validating the inhibiting effects of lutein on lipid oxidation and Maillard reaction, and the results demonstrated that it was lutein rather than lipids or their degradation products that determined the flavor formation. These findings push forward the mechanisms for the formation of meat flavor and provide insights for future manufacturing of meat aroma.

Chemerin Regulates the Proliferation and Migration of Pulmonary Arterial Smooth Muscle Cells via the ERK1/2 Signaling Pathway.

Pulmonary arterial hypertension (PAH) is an incurable disease with high mortality. Chemerin has been found to be associated with pulmonary hypertension (PH). However, the specific role of chemerin in mediating PH development remains unclear. This study aimed to elucidate the regulatory effects and the underlying mechanism of chemerin on PH and to investigate the expression levels of chemerin protein in plasma in PAH patients. In vivo, two animal models of PH were established in rats by monocrotaline (MCT) injection and hypoxia. We found that the expression levels of chemerin and its receptor, chemokine-like receptor 1 (CMKLR1), were significantly upregulated in the lungs of PH rats. Primary cultured pulmonary arterial smooth muscle cells [(PASMCs) (isolated from pulmonary arteries of normal healthy rats)] were exposed to hypoxia or treated with recombinant human chemerin, we found that CMKLR1 expression was upregulated in PASMCs in response to hypoxia or chemerin stimulation, whereas the exogenous chemerin significantly promoted the migration and proliferation of PASMCs. Notably, the regulatory effects of chemerin on PASMCs were blunted by PD98059 (a selective ERK1/2 inhibitor). Using enzyme linked immunosorbent assay (ELISA), we found that the protein level of chemerin was also markedly increased in plasma from idiopathic pulmonary arterial hypertension (IPAH) patients compared to that from healthy controls. Moreover, the diagnostic value of chemerin expression in IPAH patients was determined through receiver operating characteristic (ROC) curve analysis and the result revealed that area under ROC curve (AUC) for plasma chemerin was 0.949. Taken together, these results suggest that chemerin exacerbates PH progression by promoting the proliferation and migration of PASMCs via the ERK1/2 signaling pathway, and chemerin is associated with pulmonary hypertension.