Potato starch/naringenin complexes for high-stability Pickering emulsions: Structure, properties, and emulsion stabilization mechanism.

In this study, potato starch (PS)/naringenin (NAR) complex was prepared, and its properties and emulsification behavior were evaluated. The experimental results demonstrated that NAR successfully formed a complex with PS molecules through hydrogen bonds and other non-covalent interactions. The emulsifying capacity (ROV) of PS/NAR complex with 16 % composite ratio was 0.9999, which was higher than PS (ROV = 0.3329) (p < 0.05). Based on particle property analysis and molecular dynamics simulation, the mechanism of improving the emulsification performance might be the action of the benzene ring of NAR and intermolecular hydrogen bonding. In addition, the stability of the Pickering emulsions with PS/NAR complexes as emulgators was significantly improved. The emulsifying and rheological behavior of starch-based Pickering emulsions could be adjusted by changing the proportion of the complexes. Results demonstrated that the PS/NAR complexes might be a prospective stabilizer of Pickering emulsions based on starch material and might expand the use of PS in edible products.

Low Selenium and Low Protein Exacerbate Myocardial Damage in Keshan Disease by Affecting the PINK1/Parkin-mediated Mitochondrial Autophagy Pathway.

OBJECTIVE: Keshan disease (KD) is a myocardial mitochondrial disease closely related to insufficient selenium (Se) and protein intake. PTEN induced putative kinase 1 (PINK1)/Parkin mediated mitochondrial autophagy regulates various physiological and pathological processes in the body. This study aimed to elucidate the relationship between PINK1/Parkin-regulated mitochondrial autophagy and KD-related myocardial injury. METHODS: A low Se and low protein animal model was established. One hundred Wistar rats were randomly divided into 5 groups (control group, low Se group, low protein group, low Se + low protein group, and corn from KD area group). The JC-1 method was used to detect the mitochondrial membrane potential (MMP). ELISA was used to detect serum creatine kinase MB (CK-MB), cardiac troponin I (cTnI), and mitochondrial-glutamicoxalacetic transaminase (M-GOT) levels. RT-PCR and Western blot analysis were used to detect the expression of PINK1, Parkin, sequestome 1 (P62), and microtubule-associated proteins1A/1B light chain 3B (MAP1LC3B). RESULTS: The MMP was significantly decreased and the activity of CK-MB, cTnI, and M-GOT significantly increased in each experimental group (low Se group, low protein group, low Se + low protein group and corn from KD area group) compared with the control group (P<0.05 for all). The mRNA and protein expression levels of PINK1, Parkin and MAP1LC3B were profoundly increased, and those of P62 markedly decreased in the experimental groups compared with the control group (P<0.05 for all). CONCLUSION: Low Se and low protein levels exacerbate myocardial damage in KD by affecting the PINK1/Parkin-mediated mitochondrial autophagy pathway.

[Research progress on liposome and nanomicelle targeted drug delivery system across blood-brain barrier].

The blood-brain barrier(BBB), a protective barrier between brain tissues and brain capillaries, can prevent drugs from entering the brain tissues to exert the effect, which greatly increases the difficulty in treating brain diseases. The drug delivery system across the BBB can allow efficient drug delivery across the BBB by virtue of carriers and formulations, thereby enhancing the therapeutic effect of drugs on brain tissue diseases. Liposomes and micelles have been extensively studied with advances in the targeted therapy across the BBB for the brain due to their unique structures and drug delivery advantages. This study summarized the research status of liposome and micelle drug delivery systems across the BBB based on the literature in recent years and analyzed their application advantages and mechanism in terms of trans-BBB capability, targeting, and safety. Moreover, the problems and possible countermeasures in the research on trans-BBB liposomes and micelles were discussed according to the current clinical translation, which may provide refe-rences and ideas for the development of trans-BBB targeted nano-drugs.

Vitamin D3 alleviates cigarette smoke extract-mediated epithelial-mesenchymal transition and fibrogenesis by upregulating CC16 expression in bronchial epithelial cells.

Vitamin D3 supplementation has been previously reported to inhibit the occurrence and development of chronic obstructive pulmonary disease (COPD). However, the underlying mechanism remains unclear. Epithelial-mesenchymal transition (EMT) and fibrogenesis have been associated with the development of COPD. The aim of the present study was to investigate the potential effects and mechanism of vitamin D3 in an in vitro model of cigarette smoke (CS)-induced EMT and fibrosis, with specific focus on the role of club cell protein 16 (CC16). CS extract (CSE) at different concentrations (5, 10 and 20%) was used to treat 16-HBE cells to induce EMT and fibrogenesis following which they were treated with vitamin D3. Subsequently, the 20% CSE group was selected for further experiments, where 16-HBE cells were divided into the following five groups: The control group; the CSE group; the low-dose vitamin D3 group (250 nM); the medium-dose vitamin D3 group (500 nM); and the high-dose vitamin D3 group (1,000 nM). Western blot analysis was used to detect the protein expression levels of the EMT-related proteins E-cadherin, N-cadherin, Slug and α-SMA, fibrogenesis-related proteins collagen Ⅳ and fibronectin 1, proteins involved in the TGF-ß1/SMAD3 signaling pathway and CC16. Immunofluorescence was used to measure the protein expression levels of E-cadherin, N-cadherin and collagen Ⅳ. Specific CC16 knockdown was performed using short hairpin RNA transfection to investigate the role of CC16. The results of the present study found that vitamin D3 could increase the protein expression level of CC16 to inhibit the activation of the TGF-ß1/SMAD3 signaling pathway; thereby reducing the 20% increase in CSE-induced EMT- and fibrogenesis-related protein expression levels. Following CC16 knockdown, the inhibitory effects of vitamin D3 on EMT- and fibrogenesis-related protein expression were partially reversed. To conclude, these results suggest that vitamin D3 can inhibit the protein expression levels of EMT- and fibrogenesis-related proteins induced by CSE, at least partially through the function of CC16. These findings are expected to provide novel theoretical foundations and ideas for the pathogenesis and treatment of COPD.

Clinical Efficacy of Budesonide/Glycopyrronium Bromide/Formoterol in the Treatment of Patients with Acute Respiratory Distress Syndrome and Its Effect on Inflammatory Factors.

Objective: To examine the clinical efficacy of budesonide/glycopyrronium bromide/formoterol (Breztri Aerosphere) as an adjunct to acute respiratory distress syndrome (ARDS). Methods: A prospective study enrolled 120 patients with pulmonary endogenous ARDS admitted to the Department of Critical Care Medicine at the Fourth Hospital of Baotou from January 2017 to January 2020, and all enrollments were assigned (1 : 1) to receive conventional treatment (control group) or Breztri Aerosphere (study group). Results: Breztri Aerosphere was associated with a significantly higher total efficacy versus conventional treatment. Breztri Aerosphere resulted in significantly lower acute physiology and chronic health evaluation scoring system (APACHE II) scores and Murray lung injury scores versus conventional treatment. Both groups saw an increase in the partial pressure of carbon dioxide (PCO2), partial pressure of oxygen (PO2), and oxygen saturation (SaO2) after treatment, with higher levels seen in patients given Breztri Aerosphere. After treatment, systemic vascular resistance (SVR) in both groups rose markedly, with greater elevation witnessed in the study group. The patients given Breztri Aerosphere showed significantly lower levels of pulmonary vascular resistance (PVR), mean pulmonary arterial pressure (MAPA), pulmonary artery wedge pressure (PAWP), interleukin-6 (IL-6), interleukin-10 (IL-10), tumor necrosis factor-alpha (TNF-α), and procalcitonin (PCT) versus those receiving conventional treatment. The patients experienced shorter mechanical ventilation time and intensive care unit (ICU) time after treatment of Breztri Aerosphere versus conventional treatment. Conclusion: Adjuvant therapy with Breztri Aerosphere in ARDS can significantly lower APACHE II scores and Murray lung injury scores, improve blood gas indexes and pulmonary circulation function indexes, and shorten mechanical ventilation time and ICU time, which may be attributed to its improvement of organism inflammation status and reduction of inflammatory factors.

Liquiritin Attenuates Pathological Cardiac Hypertrophy by Activating the PKA/LKB1/AMPK Pathway.

Background: Liquiritin (LQ) is one of the main flavonoids extracted from the roots of Glycyrrhiza spp., which are widely used in traditional Chinese medicine. Studies in both cellular and animal disease models have shown that LQ attenuates or prevents oxidative stress, inflammation, and apoptosis. However, the potential therapeutic effects of LQ on pressure overload-induced cardiac hypertrophy have not been so far explored. Therefore, we investigated the cardioprotective role of LQ and its underlying mechanisms in the aortic banding (AB)-induced cardiac hypertrophy mouse model. Methods and Results: Starting 3 days after AB surgery, LQ (80 mg/kg/day) was administered daily over 4 weeks. Echocardiography and pressure-volume loop analysis indicated that LQ treatment markedly improved hypertrophy-related cardiac dysfunction. Moreover, hematoxylin and eosin, picrosirius red, and TUNEL staining showed that LQ significantly inhibited cardiomyocyte hypertrophy, interstitial fibrosis, and apoptosis. Western blot assays further showed that LQ activated LKB1/AMPKα2/ACC signaling and inhibited mTORC1 phosphorylation in cardiomyocytes. Notably, LQ treatment failed to prevent cardiac dysfunction, hypertrophy, and fibrosis in AMPKα2 knockout (AMPKα2-/-) mice. However, LQ still induced LKB1 phosphorylation in AMPKα2-/- mouse hearts. In vitro experiments further demonstrated that LQ inhibited Ang II-induced hypertrophy in neonatal rat cardiomyocytes (NRCMs) by increasing cAMP levels and PKA activity. Supporting the central involvement of the cAMP/PKA/LKB1/AMPKα2 signaling pathway in the cardioprotective effects of LQ, inhibition of Ang II-induced hypertrophy and induction of LKB1 and AMPKα phosphorylation were no longer observed after inhibiting PKA activity. Conclusion: This study revealed that LQ alleviates pressure overload-induced cardiac hypertrophy in vivo and inhibits Ang II-induced cardiomyocyte hypertrophy in vitro via activating cAMP/PKA/LKB1/AMPKα2 signaling. These findings suggest that LQ might be a valuable adjunct to therapeutic approaches for treating pathological cardiac remodeling.

Liquiritin Attenuates Lipopolysaccharides-Induced Cardiomyocyte Injury via an AMP-Activated Protein Kinase-Dependent Signaling Pathway.

Background: Liquiritin (LIQ) is a traditional Chinese medicine that has been reported to regulate inflammation, oxidative stress and cell apoptosis. However, the beneficial effects of LIQ in lipopolysaccharides (LPS)-induced septic cardiomyopathy (SCM) has not been reported. The primary goal of this study was to investigate the effects of LIQ in LPS-induced SCM model. Methods: Mice were pre-treated with LIQ for 7 days before they were injected with LPS (10 mg/kg) for inducing SCM model. Echocardiographic analysis was used to evaluate cardiac function after 12 h of LPS injection. Thereafter, mice were sacrificed to collect hearts for molecular and histopathologic assays by RT-PCR, western-blots, immunohistochemical and terminal deoxynucleotidyl transferase nick-end labeling (TUNEL) staining analysis respectively. AMPKα2 knockout (AMPKα2-/-) mice were used to elucidate the mechanism of LIQ Neonatal rat cardiomyocytes (NRCMs) treated with or without LPS were used to further investigate the roles and mechanisms of LIQ in vitro experiments. Results: LIQ administration attenuated LPS-induced mouse cardiac dysfunction and reduced mortality, based upon the restoration of EF, FS, LVEDs, heart rate, dp/dt max and dp/dt min deteriorated by LPS treatment. LIQ treatment also reduced mRNA expression of TNFα, IL-6 and IL-1ß, inhibited inflammatory cell migration, suppressed cardiac oxidative stress and apoptosis, and improved metabolism. Mechanistically, LIQ enhanced the phosphorylation of AMP-activated protein kinase α2 (AMPKα2) and decreased the phosphorylation of mTORC1, IκBα and NFκB/p65. Importantly, the beneficial roles of LIQ were not observed in AMPKα2 knockout model, nor were they observed in vitro model after inhibiting AMPK activity with an AMPK inhibitor. Conclusion: We have demonstrated that LIQ exerts its protective effects in an SCM model induced by LPS administration. LIQ reduced inflammation, oxidative stress, apoptosis and metabolic alterations via regulating AMPKα2 dependent signaling pathway. Thus, LIQ might be a potential treatment or adjuvant for SCM treatment.

Electroacupuncture improves learning and memory functions in a rat cerebral ischemia/reperfusion injury model through PI3K/Akt signaling pathway activation.

Electroacupuncture has been widely used to treat cognitive impairment after cerebral ischemia, but the underlying mechanism has not yet been fully elucidated. Studies have shown that autophagy plays an important role in the formation and development of cognitive impairment, and the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway plays an important role in autophagy regulation. To investigate the role played by the PI3K/Akt signaling pathway in the electroacupuncture treatment of cerebral ischemia/reperfusion rat models, we first established a rat model of cerebral ischemia/reperfusion through the occlusion of the middle cerebral artery using the suture method. Starting at 2 hours after modeling, electroacupuncture was delivered at the Shenting (GV24) and Baihui (GV20) acupoints, with a dilatational wave (1-20 Hz frequency, 2 mA intensity, 6 V peak voltage), for 30 minutes/day over 8 consecutive days. Our results showed that electroacupuncture reduced the infarct volume in a rat model of cerebral ischemia/reperfusion injury, increased the mRNA expression levels of the PI3K/Akt signaling pathway-related factors Beclin-1, mammalian target of rapamycin (mTOR), and PI3K, increased the protein expression levels of phosphorylated Akt, Beclin-1, PI3K, and mTOR in the ischemic cerebral cortex, and simultaneously reduced p53 mRNA and protein expression levels. In the Morris water maze test, the latency to find the hidden platform was significantly shortened among rats subjected to electroacupuncture stimulation compared with rats without electroacupuncture stimulation. In the spatial probe test, the number of times that a rat crossed the target quadrant was increased in rats subjected to electroacupuncture stimulation compared with rats without electroacupuncture stimulation. Electroacupuncture stimulation applied to the Shenting (GV24) and Baihui (GV20) acupoints activated the PI3K/Akt signaling pathway and improved rat learning and memory impairment. This study was approved by the Animal Ethics Committee of the First Affiliated Hospital of Henan University of Traditional Chinese Medicine, China (approval No. 8150150901) on March 10, 2016.

The Phospholipid:Diacylglycerol Acyltransferase-Mediated Acyl-Coenzyme A-Independent Pathway Efficiently Diverts Fatty Acid Flux from Phospholipid into Triacylglycerol in Escherichia coli.

Researchers have long endeavored to accumulate triacylglycerols (TAGs) or their derivatives in easily managed microbes. The attempted production of TAGs in Escherichia coli has revealed barriers to the broad applications of this technology, including low TAG productivity and slow cell growth. We have demonstrated that an acyl-CoA-independent pathway can divert phospholipid flux into TAG formation in E. coli mediated by Chlamydomonas reinhardtii phospholipid:diacylglycerol acyltransferase (CrPDAT) without interfering with membrane functions. We then showed the synergistic effect on TAG accumulation via the acyl-CoA-independent pathway mediated by PDAT and the acyl-CoA-dependent pathway mediated by wax ester synthase/acyl-CoA:diacylglycerol acyltransferase (WS/DGAT). Furthermore, CrPDAT led to synchronous TAG accumulation during cell growth, and this could be enhanced by supplementation of arbutin. We also showed that rationally mutated CrPDAT was capable of decreasing TAG lipase activity without impairing PDAT activity. Finally, ScPDAT from Saccharomyces cerevisiae exhibited similar activities as CrPDAT in E. coli Our results suggest that the improvement in accumulation of TAGs and their derivatives can be achieved by fine-tuning of phospholipid metabolism in E. coli Understanding the roles of PDAT in the conversion of phospholipids into TAGs during the logarithmic growth phase may enable a novel strategy for the production of microbial oils.IMPORTANCE Although phospholipid:diacylglycerol acyltransferase (PDAT) activity is presumed to exist in prokaryotic oleaginous bacteria, the corresponding gene has not been identified yet. In this article, we have demonstrated that an acyl-CoA-independent pathway can divert phospholipid flux into TAG formation in Escherichia coli mediated by exogenous CrPDAT from Chlamydomonas reinhardtii without interfering with membrane functions. In addition, the acyl-CoA-independent pathway and the acyl-CoA-dependent pathway had the synergistic effect on TAG accumulation. Overexpression of CrPDAT led to synchronous TAG accumulation during cell growth. In particular, CrPDAT possessed multiple catalytic activities, and the rational mutation of CrPDAT led to the decrease of TAG lipase activity without impairing acyltransferase activity. The present findings suggested that applying PDAT in E. coli or other prokaryotic microbes may be a promising strategy for accumulation of TAGs and their derivatives.

Pathogenesis of Metabolic Syndrome from "Qi of five Internal Organs" / 中国实验方剂学杂志

Metabolic syndrome (MS) is a group of syndromes caused by the disorder of metabolism of various substances in the body. The main clinical manifestations are dyslipidemia, central obesity, hypertension, abnormal glucose tolerance and insulin resistance. With the changes of diet structure and habits, the incidence rate of MS is increasing, and the patients are younger. It is an important factor in many diseases, such as diabetes, atherosclerosis, coronary heart disease, hyperlipidemia, cirrhosis and some cancers. MS has seriously affected people's lives and health. Central obesity and insulin resistance are recognized as important pathogenic factors. At present, the pathogenesis of MS and its components has not been fully understood. The clinical manifestations of metabolic syndrome are complex and diverse. Traditional Chinese medicine (TCM) believes that the occurrence of metabolic syndrome is related to such factors as proper diet, emotional disorders, excessive escape and little movement, old age and physical deficiency. TCM scholars have studied the pathogenesis of MS in such pathological factors as phlegm and blood stasis, such visceral functions as liver, spleen and kidney, roles of Qi and blood, and emotional factors. As the basic substance of organism, Qi is closely related to the process of metabolism. The occurrence of MS is closely related to the rise and fall of Qi moving to and from the body as well as the abnormal gasification function of the transformation of Qi. Qi is derived from the five internal organs, which are respectively called Heart Qi, liver Qi, spleen Qi, lung Qi and kidney Qi. The "Qi of the five internal organs" is involved in the whole process of the generation, transportation and excretion of the essence of the body. Based on the "Qi of five internal organs", this paper discusses the pathogenesis of MS with phlegm, blood stasis and water drink as pathological factors.

Bioactivities of serotonin transporter mediate antidepressant effects of Acorus tatarinowii Schott.

ETHNOPHARMACOLOGICAL RELEVANCE: Acrorus tatarinowii Schott has been widely used in the treatments of neuropsychiatric and digestive disorders in clinical practices of traditional Chinese medicine for thousands of years. Both clinical and preclinical studies demonstrated antidepressant effects of A. tatarinowii. However, the possible action mechanisms of antidepressant effects of A. tatarinowii remain unraveled. AIM OF THE STUDY: The present study aimed to investigate the roles of serotonin transporter (SERT) in antidepressant effects of A. tatarinowii. MATERIALS AND METHODS: Antidepressant effects of water extract of A. tatarinowii were evaluated by forced swimming test (FST), tail suspension test (TST) and locomotor activity test. The water extract was analyzed by ultra high performance liquid chromatography (UPLC) method. Two major fractions of A. tatarinowii, petroleum ether extract and water extract after petroleum ether processed, were prepared and analyzed by UPLC method. Further, volatile oil extracted by ether extraction, solid phase micro-extraction (SPME) and hydro-distillation were compared and analyzed by gas chromatography-mass spectrometer (GC-MS) method. Finally, major constituents of water extract of A. tatarinowii were isolated by preparative high performance liquid chromatography (HPLC) and identified by extensive spectroscopic analyses. Effects of all of the above mentioned samples on SERT activity were tested by a high content assay (HCA). RESULTS: Results of FST, TST and locomotor activity confirmed that water extract of A. tatarinowii significantly decreased mice immobility time but did not change mice locomotor activity. UPLC analysis results revealed that the water extract contained trace amount of ß-asarone (0.0004206%) and α-asarone (0.0001918%). HCA results demonstrated that the water extract significantly enhanced SERT activity at 100 µg/mL. Further, GC-MS and UPLC analyses revealed that petroleum ether extract contained high content of ß-asarone (45.63%) and α-asarone (12.50%). GC-MS analysis results demonstrated that the volatile oil extracted by ether extraction, SPME and hydro-distillation contained similar major components. HCA results verified that the petroleum ether extract significantly enhanced SERT activity at 1.56 µg/mL. Moreover, UPLC analysis of water extract after petroleum ether processed did not show any characteristic peaks. HCA results demonstrated that this extract significantly inhibited SERT activity at 50-100 µg/mL. Finally, phytochemistry investigation on the water extract of A. tatarinowii afforded seven constituents including veratric acid (9), anisic acid (7), 3,4,5-trimethoxybenzoic acid (3), trans-isoferulic acid (2), 2,4,5-trimethoxybenzoic acid (11), 4-hydroxybenzoic acid (6) and syringic acid (13). Their structures were established on the basis of nuclear magnetic resonance (NMR) and mass spectrometer (MS) data and comparative UPLC analyses. HCA results demonstrated the major components of the water extract of A. tatarinowii demonstrated SERT enhancement/inhibition activities. CONCLUSIONS: This study first systematically demonstrated the roles of SERT activity in antidepressant effects of A. tatarinowii, including water extract, major fractions and main constituents. These results revealed that A. tatarinowii could regulate SERT activities in bidirectional ways.

Icariside II attenuates cardiac remodeling via AMPKα2/mTORC1 in vivo and in vitro.

Icariside II (ICA II), a flavonoid derived from Epimediumbrevicormum Maxin in, has multiple biological activities in Chinese traditional medicine. Our study aimed to investigate the potential activity of ICA II against cardiac remodeling and the underlying mechanism. Mice received aorta banding (AB) or sham surgery, and then were randomly divided into ICA II or vehicle (veh) group for 6 weeks. After echocardiography and pressure-volume loop examination, hearts were harvested for histopathological analysis and molecular mechanism investigation. Additionally, neonatal rat cardiomyocytes (NRCM) were used for in vitro experiments. ICA II attenuated the systolic and diastolic cardiac dysfunction, and protected mouse heart from hypertrophy and fibrosis. The underlying mechanism might involve in the regulation of Akt, AMPKα and mTORC. In in vitro experiment, ICA II prevented phenylephrine (PE) induced NRCM hypertrophy by regulating AMPKα/mTORC pathway. This protective effect was disappeared after treatment with Compound C (CpC), an AMPKα inhibitor. Moreover, ICA II activated AMPK at baseline. ICAII was superior to resveratrol in activating AMPKα and similar to AICAR. ICA II protected against cardiac remodeling and NRCM hypertrophy by regulating AMPK/mTORC pathway. ICA II may be a candidate for the treatment of malignant cardiac remodeling.

[Synthesis and identification of artificial antigen of spinosin].

Immunogenic antigen (spinosin-BSA) and coating antigen (spinosin-OVA) of spinosin were synthesized by sodium periodate oxidation method. UV scanning analysis method showed that these two spinosins were successfully conjugated with carrier protein and the coupling ratio was 17 and 13.7, respectively. Meanwhile, when immunized by spinosin-BSA，the mice can produce anti-spinosin antibodies with the high titer (1:32 000),specificity (IC50 211.6 µg·L⁻¹) and low cross-reaction rate measured by ELISA tests. The artificial antigen of spinosin was successfully synthesized, which can be applied for preparation of monoclonal antibodies and establishment of appropriate immune method.

Myricetin attenuated LPS induced cardiac injury in vivo and in vitro.

Sepsis induced myocardial dysfunction (SIMD) is a common complication and leads to an increased mortality. SIMD is closely related to inflammation and oxidative stress. Myricetin exhibits strong capacities of anti-inflammation and anti-oxidative stress, but its pharmacological effects for lipopolysaccharide (LPS) induced cardiac injury remains undefined. This study aimed to explore whether myricetin was efficient to alleviate SIMD in mice and neonatal rat cardiomyocytes injury. Mice administrated with myricetin (100 mg/kg, po, bid) or vehicle groups were challenged with LPS (10 mg/kg, ip), and cardiac functions examined by echocardiography after 12 hr LPS exposure. LPS markedly impaired mouse cardiac functions, which were significantly attenuated by myricetin administration. Myricetin significantly reduced the production of inflammatory cytokines both in serum and cardiac tissue. Myricetin could inhibit the nuclear translocation of p65, degradation of IκBα, and cellular apoptosis in vivo and in vitro. Myricetin also prevented overexpression of iNOS and reduction of oxidoreductase (SOD and GPx) activity. Besides, Myricetin treatment could attenuate production of inflammatory cytokines of peritoneal macrophages stimulated with LPS in vitro. Thus we concluded that myricetin could attenuate the LPS induced cardiac inflammation injury in vivo and in vitro. Myricetin may be a potential therapy or adjuvant therapy for SIMD.

Kaempferol Attenuates Cardiac Hypertrophy via Regulation of ASK1/MAPK Signaling Pathway and Oxidative Stress.

Kaempferol has been demonstrated to provide benefits for the treatment of atherosclerosis, coronary heart disease, hyperlipidemia, and diabetes through its antioxidant and anti-inflammatory properties. However, its role in cardiac hypertrophy remains to be elucidated. The aim of our study was to investigate the effects of kaempferol on cardiac hypertrophy and the underlying mechanism. Mice subjected to aorta banding were treated with or without kaempferol (100 mg/kg/d, p. o.) for 6 weeks. Echocardiography was performed to evaluate cardiac function. Mice hearts were collected for pathological observation and molecular mechanism investigation. H9c2 cardiomyocytes were stimulated with or without phenylephrine for in vitro study. Kaempferol significantly attenuated cardiac hypertrophy induced by aorta banding as evidenced by decreased cardiomyocyte areas and interstitial fibrosis, accompanied with improved cardiac functions and decreased apoptosis. The ASK1/MAPK signaling pathways (JNK1/2 and p38) were markedly activated in the aorta banding mouse heart but inhibited by kaempferol treatment. In in vitro experiments, kaempferol also inhibited the activity of ASK1/JNK1/2/p38 signaling pathway and the enlargement of H9c2 cardiomyocytes. Furthermore, our study revealed that kaempferol could protect the mouse heart and H9c2 cells from pathological oxidative stress. Our investigation indicated that treatment with kaempferol protects against cardiac hypertrophy, and its cardioprotection may be partially explained by the inhibition of the ASK1/MAPK signaling pathway and the regulation of oxidative stress.

[Investigation of the potentially effective components of Semen Ziziphi Spinosae based on "in vitro to in vivo" translation approach].

The study aims to investigate the effective components of Semen Ziziphi Spinosae (SZR) in nourishing the heart and tranquilizing the mind. A method of ultra high liquid chromatography (UHPLC) coupled with Q Exactive high resolution mass spectrometry (HR-MS) was developed. Based on the UV spectra, retention time and MS spectra, 25 compounds of SZR extract were identified or tentatively characterized, including 12 flavonoids, 8 triterpenoids saponins, 2 fatty acid and 3 alakoids. The study illuminated the major chemical components. Twenty bioactive components were determined in rat urine after oral administration of SZR extract by "in vitro to in vivo" translation approach, including 16 prototype compounds and 4 metabolites. Spinosin, swertisin, jujuboside A and B were considered as the effective and active constituents in SZR of the sedative and hypnotic effects, which emodies characteristics of multiple components. It was beneficial exploration for searching the effective and active constituents of SZR in nourishing the heart and tranquilizing the mind.

High-performance size-exclusion chromatography studies on the formation and distribution of polar compounds in camellia seed oil during heating.

Camellia seed oil (CSO) is rich in oleic acid and has a high number of active components, which give the oil high nutritional value and a variety of biological activity. The aim of the present study was to determine the changes in the content and distribution of total polar compounds (TPC) in CSO during heating. TPC were isolated by means of preparative flash chromatography and further analyzed by high-performance size-exclusion chromatography (HPSEC). The TPC content of CSO increased from 4.74% to 25.29%, showing a significantly lower formation rate as compared to that of extra virgin olive oil (EVOO) and soybean oil (SBO) during heating. Furthermore, heating also resulted in significant differences (P<0.05) in the distribution of TPC among these oils. Though the content of oxidized triacylglycerol dimers, oxidized triacylglycerol oligomers, and oxidized triacylglycerol monomers significantly increased in all these oils, their increased percentages were much less in CSO than those in EVOO, indicating that CSO has a greater ability to resist oxidation. This work may be useful for the food oil industry and consumers in helping to choose the correct oil and to decide on the useful lifetime of the oil.

Caffeoyl Triterpenoid Esters as Potential Anti-ischemic Stroke Agents from Celastrus orbiculatus.

Three new triterpenoids, celastrusins A-C (1-3), together with 3-O-caffeoyl-α-amyrin (4) were isolated from the root bark of Celastrus orbiculatus. Their structures were identified by spectroscopic analysis, X-ray crystallography using Cu Kα radiation, and the comparison of both observed and reported spectroscopic data. An in vitro bioassay revealed that the caffeoyl triterpenoid esters 1, 3, and 4 possess neuroprotective effects against oxygen-glucose deprivation (OGD) induced SH-SY5Y cell damage. Further animal studies indicated that compound 1 significantly reduced brain infarction after transient middle cerebral artery occlusion (MCAO) in rats using a 10 mg/kg (i.v.) dose.

Observations on the Efficacy of Electroacupuncture at Points Gongsun and Neiguan in Treating Functional Dyspepsia / 上海针灸杂志

Objective To investigate the clinical efficacy of electroacupuncture at points Gongsun and Neiguan in treating functional dyspepsia.Methods Sixty-two patients with functional dyspepsia were randomly allocated to a treatment group of 32 cases and a control group of 30 cases. The treatment group received electroacupuncture at points Gongsun and Neiguan and the control group took mosapride citrate dispersible tablets. The clinical symptoms were observed, electrogastrography was performed and the Functional Dyspepsia Diseases Quality of Life (FDDQL) score were recorded in the two groups before and after treatment. The clinical therapeutic effects were compared between the two groups.Results There were statistically significant differences in the total efficacy rates for the clinical symptoms between the treatment and control groups (P<0.05). There were statistically significant pre-/post-treatment differences in postprandial electrogastrographic main wave and slow wave frequencies in the two groups (P<0.05). There were statistically significant post-treatment differences in postprandial electrogastrographic main wave and slow wave frequencies between the treatment and control groups (P<0.05). There were statistically significant pre-/post-treatment differences in the FDDQL subscores in the treatment groups (P<0.05). There were statistically significant post-treatment differences in the FDDQL subscores between the treatment and control groups (P<0.05).Conclusions Electroacupuncture at points Gongsun and Neiguan is an effective way to treat functional dyspepsia. It can improve the clinical symptoms and regulate gastrointestinal rhythm in the patients.

[Isolation and characterization of two bacteria with heavy metal resistance and phosphate solubilizing capability].

Two phosphate solubilizing bacteria (T PSB1 and T PSB 2) with high heavy metal resistance were isolated from soil of a lead-zinc mine in Huayuan of Hunan Province, China. These two bacteria were identified as Stenotrophomonas maltophilia and Burkholderia gladioli by 16S rRNA sequencing analysis, respectively. In the media containing insoluble inorganic calcium phosphate, the soluble phosphate amounts reached respectively 402.9 mg x L(-1) and 589.9 mg x L(-1) with the bacteria T PSB1 and T PSB2 after two weeks' growth. Moreover, the two bacteria developed solubilizing halos on the plates supplemented with the organic phosphate compounds, and the resulting soluble phosphate amounts in the broth media were respectively 2.97 mg x L(-1) and 4.69 mg x L(-1). In addition, these two bacteria showed the resistance to up to 2000 mg x L(-1) Zn2+, and their phosphate solubilizing amounts reached respectively 114.8 mg x L(-1) and 125.1 mg x L(-1). Similarly, their heavy metal resistance and phosphate solubilizing ability were also found in the Cr and Pb broth media with the concentration of 1000 mg x L(-1). In the Pb media, the soluble phosphate amounts reached respectively 57.9 mg x L(-1) and 71.7 mg x L(-1), and the soluble P amounts in the Cr media were 60.1 mg x L(-1) and 98.4 mg x L(-1) at the concentration of 1000 mg x L(-1).