Ultra-Wideband Positioning Sensor with Application to an Autonomous Ultraviolet-C Disinfection Vehicle.

Due to the COVID-19 virus being highly transmittable, frequently cleaning and disinfecting facilities is common guidance in public places. However, the more often the environment is cleaned, the higher the risk of cleaning staff getting infected. Therefore, strong demand for sanitizing areas in automatic modes is undoubtedly expected. In this paper, an autonomous disinfection vehicle with an Ultraviolet-C (UVC) lamp is designed and implemented using an ultra-wideband (UWB) positioning sensor. The UVC dose for 90% inactivation of the reproductive ability of COVID-19 is 41.7 J/m2, which a 40 W UVC lamp can achieve within a 1.6 m distance for an exposure time of 30 s. With this UVC lamp, the disinfection vehicle can effectively sterilize in various scenarios. In addition, the high-accuracy UWB positioning system, with the time difference of arrival (TDOA) algorithm, is also studied for autonomous vehicle navigation in indoor environments. The number of UWB tags that use a synchronization protocol between UWB anchors can be unlimited. Moreover, this proposed Gradient Descent (GD), which uses Taylor method, is a high-efficient algorithm for finding the optimal position for real-time computation due to its low error and short calculating time. The generalized traversal path planning procedure, with the edge searching method, is presented to improve the efficiency of autonomous navigation. The average error of the practical navigation demonstrated in the meeting room is 0.10 m. The scalability of the designed system to different application scenarios is also discussed and experimentally demonstrated. Hence, the usefulness of the proposed UWB sensor applied to UVC disinfection vehicles to prevent COVID-19 infection is verified by employing it to sterilize indoor environments without human operation.

Protective Effect of Silibinin on Lipopolysaccharide-Induced Endotoxemia by Inhibiting Caspase-11-Dependent Cell Pyroptosis.

OBJECTIVE: To explore the protective effect and the underlying mechanism of silibinin (SIB), one of the active compounds from Silybum marianum (L.) Gaertn in endotoxemia. METHODS: Mouse peritoneal macrophage were isolated via intraperitoneally injection of BALB/c mice with thioglycolate medium. Cell viability was assessed using the cell counting kit-8, while cytotoxicity was determined through lactate dehydrogenase cytotoxicity assay. The protein expressions of interleukin (IL)-1 α, IL-1 ß, and IL-18 were determined by enzyme-linked immunosorbent assay. Intracellular lipopolysaccharide (LPS) levels were measured by employing both the limulus amoebocyte lysate assay and flow cytometry. Additionally, proximity ligation assay was employed for the LPS and caspase-11 interaction. Mice were divided into 4 groups: the control, LPS, high-dose-SIB (100 mg/kg), and low-dose-SIB (100 mg/kg) groups (n=8). Zebrafish were divided into 4 groups: the control, LPS, high-dose-SIB (200 εmol/L), and low-dose-SIB (100 εmol/L) groups (n=30 for survival experiment and n=10 for gene expression analysis). The expression of caspase-11, gasdermin D (GSDMD), and N-GSDMD was determined by Western blot and the expressions of caspy2, gsdmeb, and IL-1 ß were detected using quantitative real-time PCR. Histopathological observation was performed through hematoxylineosin staining, and protein levels in bronchoalveolar lavage fluid were quantified using the bicinchoninicacid protein assay. RESULTS: SIB noticeably decreased caspase-11 and GSDMD-mediated pyroptosis and suppressed the secretion of IL-1 α, IL-1 ß, and IL-18 induced by LPS (P<0.05). Moreover, SIB inhibited the translocation of LPS into the cytoplasm and the binding of caspase-11 and intracellular LPS (P<0.05). SIB also attenuated the expression of caspase-11 and N-terminal fragments of GSDMD, inhibited the relative cytokines, prolonged the survival time, and up-regulated the survival rate in the endotoxemia models (P<0.05). CONCLUSIONS: SIB can inhibit pyroptosis in the LPS-mediated endotoxemia model, at least in part, by inhibiting the caspase-11-mediated cleavage of GSDMD. Additionally, SIB inhibits the interaction of LPS and caspase-11 and inhibits the LPS-mediated up-regulation of caspase-11 expression, which relieves caspase-11-dependent cell pyroptosis and consequently attenuates LPS-mediated lethality.

Electrophilic components from Xiaoheiyao (rhizomes of Inula nervosa Wall.) alleviate the production of heterocyclic aromatic amines via creatinine inhibition.

Xiaoheiyao is the rhizome of Inula nervosa Wall., a traditional spice and medicinal herb in China. In this study, the creatinine inhibitor from Xiaoheiyao extract and also the effects and mechanism on the production of heterocyclic aromatic amines (HAAs) were investigated. Xiaoheiyao extract inhibited the total contents of seven detected HAAs in grilled beef patties, particularly aminoimidazole-azaarenes (AIAs) in a dose-dependent manner, reaching a maximum inhibition rate of 62% for total HAAs and 73% for AIAs. The most effective subfraction of Xiaoheiyao extract (IER80) contained abundant potential creatinine inhibitors, as revealed by immobilized creatinine probe, HPLC and UPLC-MS/MS analyses. Moreover, electrophilic p-coumaric acid derivatives were discovered from IER80 by feature based molecular networking. p-Coumaric acid was demonstrated to inhibit the contents of total HAAs and AIAs in grilled beef patties and model system. Quantitative analyses of the precursor and intermediates of AIAs in model system revealed that p-coumaric acid mainly affected the generation of AIAs by inhibiting creatinine.

Effect of Sugar and Milk Powder Addition on the Mechanical Properties and Texture of Chocolate.

In order to investigate how the addition of two common ingredients in chocolate, sugar and milk powder, affects the mechanical properties of solid chocolate, uniaxial compression tests and wedge fracture tests were carried out using four ratios of chocolate as the experimental material. Mechanical properties such as Young's modulus and fracture toughness were directly correlated with textural properties such as hardness, elasticity, and brittleness. The results show that adding sugar increases Young's modulus and fracture toughness of chocolate, while milk powder is the opposite. In equal amounts of both, sugar played a more substantial role. In combination with the properties exhibited by chocolate in the above tests, data from creep tests were collected to improve the classical Bingham model and develop a new constitutive model for predicting the mechanical behaviour of solid chocolate with different ratios of added sugar and milk powder. The new four-component constitutive model allows for a more accurate fit to the creep test data and this work provides some suggestions for making different tasting chocolates by adjusting the addition of ingredients.

Emodin Protects Against Lipopolysaccharide-Induced Acute Lung Injury via the JNK/Nur77/c-Jun Signaling Pathway.

Background: Acute lung injury (ALI) is a serious inflammatory disease with clinical manifestations of hypoxemia and respiratory failure. Presently, there is no effective treatment of ALI. Although emodin from Rheum palmatum L. exerts anti-ALI properties, the underlying mechanisms have not been fully explored. Purpose: This study aimed to investigate the therapeutic effect and mechanism of emodin on LPS-induced ALI in mice. Methods: RAW264.7 cells and zebrafish larvae were stimulated by LPS to establish inflammatory models. The anti-inflammatory effect of emodin was assessed by ELISA, flow cytometric analysis, and survival analysis. In vitro mechanisms were explored by using Western blotting, luciferase assay, electrophoretic mobility shift assay (EMSA), and small interfering RNA (siRNA) approach. The acute lung injury model in mice was established by the intratracheal administration of LPS, and the underlying mechanisms were assessed by detecting changes in histopathological and inflammatory markers and Western blotting in lung tissues. Results: Emodin inhibited the inflammatory factor production and oxidative stress in RAW264.7 cells, and prolonged the survival of zebrafish larvae after LPS stimulation. Emodin suppressed the expression levels of phosphorylated JNK at Thr183/tyr182 and phosphorylated Nur77 at Ser351 and c-Jun, and increased the expression level of Nur77 in LPS-stimulated RAW264.7 cells, while these regulatory effects of emodin on Nur77/c-Jun were counteracted by JNK activators. The overexpression of JNK dampened the emodin-mediated increase in Nur77 luciferase activity and Nur77 expression. Moreover, the inhibitory effect of emodin on c-Jun can be attenuated by Nur77 siRNA. Furthermore, emodin alleviated LPS-induced ALI in mice through the regulation of the JNK/Nur77/c-Jun pathway. Conclusions: Emodin protects against LPS-induced ALI through regulation on JNK/Nur77/c-Jun signaling. Our results indicate the potential of emodin in the treatment of ALI.

The Alleviation of Dextran Sulfate Sodium (DSS)-Induced Colitis Correlate with the logP Values of Food-Derived Electrophilic Compounds.

Food-derived electrophilic compounds (FECs) are small molecules with electrophilic groups with potential cytoprotective effects. This study investigated the differential effects of six prevalent FECs on colitis in dextran sodium sulfate (DSS)-induced mice and the underlying relationship with molecular characteristics. Fumaric acid (FMA), isoliquiritigenin (ISO), cinnamaldehyde (CA), ferulic acid (FA), sulforaphane (SFN), and chlorogenic acid (CGA) exhibited varying improvements in colitis on clinical signs, colonic histopathology, inflammatory and oxidative indicators, and Nrf2 pathway in a sequence of SFN, ISO > FA, CA > FMA, CGA. Representative molecular characteristics of the "penetration-affinity−covalent binding" procedure, logP value, Keap1 affinity energy, and electrophilic index of FECs were theoretically calculated, among which logP value revealed a strong correlation with colitis improvements, which was related to the expression of Nrf2 and its downstream proteins. Above all, SFN and ISO possessed high logP values and effectively improving DSS-induced colitis by activating the Keap1−Nrf2 pathway to alleviate oxidative stress and inflammatory responses.

Inhibition of the STAT3 Signaling Pathway Contributes to the Anti-Melanoma Activities of Shikonin.

BACKGROUND: Malignant melanoma is an extremely aggressive and metastatic cancer, and highly resistant to conventional therapies. Signal transducer and activator of transcription 3 (STAT3) signaling promotes melanoma development and progression, which has been validated as an effective target in melanoma treatment. Natural naphthoquinone shikonin is reported to exert anti-melanoma effects. However, the underlying mechanisms have not been fully elucidated. PURPOSE: This study aims to evaluate the anti-melanoma activities of shikonin and explore the involvement of STAT3 signaling in these effects. METHODS: Zebrafish tumor model was established to evaluate the anti-human melanoma effects of shikonin in vivo. MTT assay and colony formation assay were employed to investigate the anti-proliferative effects of shikonin on human melanoma A375 and A2058 cells. Flow cytometry was used to analyze cell cycle distribution and apoptosis induction. Wound healing assay and Transwell chamber assay were conducted to examine the cell migratory and invasive abilities. Immunofluorescence assay was used to observe F-actin, Tubulin, and STAT3 localization. Western blotting was used to determine the expression levels of proteins associated with apoptosis and key proteins in the STAT3 signaling pathway. Immunoblotting was performed in DSS cross-linked cells to determine the homo-dimerization of STAT3. Gelatin zymography was employed to evaluate the enzymatic activity of MMP-2 and MMP-9. Transient transfection was used to overexpress STAT3 in cell models. RESULTS: Shikonin suppressed melanoma growth in cultured cells and in zebrafish xenograft models. Shikonin induced melanoma cells apoptosis, inhibited cell migration and invasion. Mechanistic study indicated that shikonin inhibited the phosphorylation and homo-dimerization of STAT3, thus reduced its nuclear localization. Further study showed that shikonin decreased the levels of STAT3-targeted genes Mcl-1, Bcl-2, MMP-2, vimentin, and Twist, which are involved in melanoma survival, migration, and invasion. More importantly, overexpression of constitutively active STAT3 partially abolished the anti-proliferative, anti-migratory, and anti-invasive effects of shikonin. CONCLUSION: The anti-melanoma activity of shikonin is at least partially attributed to the inhibition on STAT3 signaling. These findings provide new insights into the anti-melanoma molecular mechanisms of shikonin, suggesting its potential in melanoma treatment.

Geniposide Enhances Macrophage Autophagy through Downregulation of TREM2 in Atherosclerosis.

Macrophage autophagy defect is closely related to the progression of atherosclerosis (AS) and is regulated by the triggering receptor expressed on myeloid cell 2 (TREM2). TREM2 is a key factor in the development of Alzheimer's disease (AD), the deficiency of which leads to anomalous autophagy in microglia. However, the role of TREM2 in the autophagy of plaque macrophages is still unclear. Geniposide (GP) can inhibit AS progression and enhance macrophage autophagy, although the underlying mechanisms remain unknown. We found that high-fat diet (HFD) feeding significantly increased TREM2 levels and inhibited autophagy in the macrophages of ApoE[Formula: see text] mice. TREM2 overexpression in RAW264.7 macrophages decreased autophagy via activation of mTOR signaling. GP inhibited the progression of AS in ApoE[Formula: see text] mice, reinforced macrophage autophagy, and downregulated TREM2 by inhibiting mTOR signaling. Taken together, augmenting the autophagy levels in plaque macrophages by inhibiting the TREM2/mTOR axis can potentially impede atherosclerotic progression. The promising therapeutic effects of GP seen in this study should be validated in future trials, and the underlying mechanisms have to be elucidated in greater detail.

Protection of a polysaccharide from Salvia miltiorrhiza, a Chinese medicinal herb, against immunological liver injury in mice.

This study was designed to evaluate the hepatoprotective effects of S. miltiorrhiza polysaccharides (SMPS) in immunological liver injury induced by Bacille-Calmette-Guerin (BCG) and lipopolysaccharide (LPS) in mice. SMPS effectively improved the liver index, spleen index and thymus index, reduced the serum levels of alanine aminotransferase, aspartate aminotransferase and nitric oxide, and restored liver homogenate contents of tumor necrosis factor-alpha and interleukin-1beta. The histopathological analysis suggested that SMPS reduced the degree of liver injury. The results suggest that SMPS play a protective role against immunological liver injury, which may have important implications for our understanding on the immunoregulatory mechanisms of polysaccharides.

Liang-Ge-San, a classic traditional Chinese medicine formula, protects against lipopolysaccharide-induced inflammation through cholinergic anti-inflammatory pathway.

Liang-Ge-San (LGS) is a classic formula in traditional Chinese medicine, which is widely used to treat acute lung injury (ALI), pharyngitis and amygdalitis in clinic. However, the underlying mechanisms remain poorly defined. In this study, we discovered that LGS exerted potent anti-inflammatory effects in lipopolysaccharide (LPS)-induced inflammation. We found that LGS significantly depressed the production of IL-6 and TNF-α in LPS-stimulated RAW 264.7 macrophage cells. The degradation and phosphorylation of IκBα and the nuclear translocation of NF-κB p65 were also inhibited. Moreover, LGS activated α7 nicotinic cholinergic receptor (α7nAchR). The blockage of α7nAchR by selective inhibitor methyllycaconitine (MLA) or α7nAchR siRNA attenuated the inhibitory effects of LGS on IκBα, NF-κB p65, IL-6 and TNF-α. Critically, LGS significantly inhibited inflammation in LPS-induced ALI rats through the activation of NF-κB signaling pathway. However, these protective effects could be counteracted by the treatment of MLA. Taken together, we first demonstrated anti-inflammatory effects of LGS both in vitro and in vivo through cholinergic anti-inflammatory pathway. The study provides a rationale for the clinical application of LGS as an anti-inflammatory agent and supports the critical role of cholinergic anti-inflammatory pathway in inflammation.

Trichosanatine alleviates oxidized low-density lipoprotein induced endothelial cells injury via inhibiting the LOX-1/p38 MAPK pathway.

The LOX-1/p38 mitogen-activated protein kinase (MAPK) pathway has been proved to participate in the endothelial dysfunction in atherosclerosis. Trichosanatineis is an active compound isolated from the peel of Trichosanthes kirilowii. This study aims to determine whether trichosanatine prevents the oxidized low-density lipoprotein (ox-LDL)-induced insult through inhibition of the LOX-1/p38 MAPK pathway in HUVECs. HUVECs were treated with 150 mg/ml ox-LDL for 24 h to establish an ox-LDL-induced endothelial injury model. Cell viability, mitochondrial membrane potential (MMP), apoptosis, reactive oxygen species (ROS) level, LOX-1 and p38 MAPK expression level were measured. The results indicated that HUVECs were pretreated with either 100 mM trichosanatine or LOX-1 shRNA prior to exposure to ox-LDL for 24 h. Exposure of HUVECs to 150 mg/ml ox-LDL for 24 h significantly up-regulated the expression levels of LOX-1. The increased expression levels of LOX-1 were markedly attenuated by pretreatment with 100 mM trichosanatine. In addition, the ox-LDL-induced increase in phosphorylated (p) p38 MAPK expression was ameliorated by pretreatment with LOX-1 shRNA. Pretreatment of HUVECs with either trichosanatine or LOX-1 shRNA before exposure to ox-LDL significantly inhibited the ox-LDL-induced injuries, as evidenced by an increase in cell viability, a decrease in apoptotic cells, a ROS generation and a loss of MMP. In conclusion, we have demonstrated for the first time that the LOX-1/p38 MAPK pathway contributes to the ox-LDL-induced injury in HUVECs. Meanwhile, the trichosanatine protects the HUVECs against ox-LDL-induced injury at least in part by inhibiting the activated of LOX-1/p38 MAPK pathway.

[Effect of Buyanghuanwu decoction on neuronal nitric oxide synthase expression after permanent focal cerebral ischemia in rats].

OBJECTIVE: To observe the effect of Buyanghuanwu decoction (BYHWD) on neuronal nitric oxide synthase (nNOS) immunoreactivity after permanent focal cerebral ischemia in rats. METHODS: The rats were randomized into normal control group, cerebral ischemia model groups (with ischemia for 1, 4, and 10 h respectively), and corresponding ischemia groups treated with BYHWD. Focal cerebral ischemia was produced by permanent middle cerebral artery occlusion (MCAO) with nylon suture inserted through the internal carotid artery. Brain nNOS in different brain regions was assayed by SABC immunohistochemistry at different time points ranging from 1 to 10 h after occlusion. RESULTS: nNOS activity in the cerebral tissues was enhanced in the ischemic hemisphere as the time following ischemia prolonged. Pretreatment with BYHWD group significantly decreased nNOS activity to 170.80+/-21.71 and 189.20+/-18.53 in the striatum cortex 18a region and to 127.33+/-19.83, 215.20+/-38.80, and 191.20+/-22.39 in the caudate putamen, in comparison with the untreated cerebral ischemia model group (244.60+/-12.44 and 363.00+/-24.82 in the striatum cortex 18a region and 138.67+/-13.99, 266.40+/-29.25, and 373.20+/-31.55 in the caudate putamen, P<0.05), and this effect began to be observed in the early stage of ischemia and gradually high-lighted as the ischemia time increased. CONCLUSION: BYHWD significantly restrains the up-regulated activity of nNOS after focal cerebral ischemia to protect the cerebral ischemic lesion from the early stage following the onset of ischemia.

Tests of the pharmacodynamics and toxicity of Duliang capsule.

OBJECTIVE: To study the analgesic efficacy, toxicity and impact of Duliang capsule (DLC) and Duliang pill (DLP), different dosage forms of a patent Chinese herbal medicine, on the hemodynamics in mice and rats. METHODS: In hotplate and writhing tests in mice, the effects of both drugs on the latency of paw-licking response and the writhing number of times were observed. The changes of blood viscosity in rat models of blood stasis were measured with Viscometer-R80, and acute and chronic toxicity of DLC observed. RESULTS: DLP at the dose of 5 g/kg.b.w. and DLC at 10, 5 or 3 g/kg.b.w. significantly prolonged the latency of paw-licking response and reduced writhing times. The analgesic effects of DLC and DLP occurred 0.5 and 1 h respectively after the administration, and they could both lower the viscosity of the whole blood and hematocrit level in the blood-stasis rat models. Toxicity of the drug was not observed in acute or chronic toxicity tests. CONCLUSIONS: Both DLC and DLP possess strong analgesic effect and can lower blood viscosity and hematocrit, but DLC takes effect sooner than DLP as analgesics and can be effectively and safely applied clinically.

[Effects of Buyanghuanwu decoction (BYHWT) on proliferation of cultured rat cortical neurons].

OBJECTIVE: To observe the effect of rat serum containing Buyanghuanwu decoction (BYHWT) on the proliferation of cultured rat cortical neurons, so as to understand the mechanism of BYHWT in the treatment of hypoxia brain damage. METHODS: The growth of cultured rat cortical neurons were observed by MTT assay to evaluate the effect of the serum containing BYHWT on the neurons cultured in both normal and hypoxia conditions. RESULTS: BYHWT significantly promoted proliferation of the neurons cultured under both normal and hypoxia conditions, in comparison with the response of the cells to drug-free serum (P<0.05). CONCLUSION: Some of the constituents of BYHWT in rat serum can promote the proliferation of rat cortical neurons cultured in both normal and hypoxia conditions.

[Protective effect of Buyanghuanwu Tang on cultured rat cortical neurons against hypoxiainduced apoptosis].

OBJECTIVE: To investigate the protective effect of Buyanghuanwu Tang (BYHWT), a decoction with 6 herbal ingredients, on in vitro cultured rat cortical neurons against apoptosis induced by hypoxia, and study its effect on the production of nitric oxide (NO) and oxygen free radicals and Bcl-2 expression in the neurons during hypoxia. METHODS: Models of hypoxia-induced neuron apoptosis were established and treated with sera containing BYHWT. Stained by propidium iodide, the neurons underwent apoptosis analysis using flow cytometry, and the levels of malonyl dialdehyde (MDA) and NO were measured with spectrophotometer, with Bcl-2 expression assayed by immunohistochemical method with flow cytometry. RESULTS: In BYHWT-treated neurons, apoptosis rates were significantly lower than those of the neurons subjected to hypoxia exclusively, and at the same time NO and MDA production was remarkably reduced. Bcl-2 expression, however, was up-regulated. CONCLUSION: BYHWT can protect neurons from hypoxia-induced apoptosis, the mechanism of which may lie in the elimination of NO and oxygen free radicals produced during hypoxia and up-regulation of Bcl-2 expression.

Effects of gentiopicrooside injections on experimental hepatic injury.

OBJECTIVE: To investigate the protective and jaundice-relieving effects of gentiopicrooside (GPS) injections in mouse and rat models of chemical-induced and immune-mediated hepatic injury. METHODS: Mouse models of chemical-induced liver injury were established by CCl4 injections into the abdominal cavity, mouse models of immune-mediated liver damage by bacillus Calmette-Guerin (BCG) and lipopolysaccharide (LPS) and rat models of jaundice by oral alpha-naphthyliso-thiocyanate (ANIT). Treatment with GPS injections was administered and both of enzyme activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in the Serum were measured in the models. The serum level of total bilirubin was determined in the jaundice models. RESULTS: Compared with those of the untreated models, the enzyme activities of ALT and AST were significantly reduced in groups with a 10 day GPS treatment (P<0.001, P<0.05). Higher dosage of GPS showed more conspicuous effects in relieving the jaundice. CONCLUSION: GPS can be administered as the antagonist against CC14-induced liver injury and offers protection against immune-mediated liver damage.

[The effect of niaoduqing tablet on the diuresis in normal rats and the hemorheology in blood-stasis rats].

OBJECTIVE: To observe the effect of the Niaoduqing Tablet(NDT) on the diuresis in normal rats and the hemorheology in rats of blood stasis and compare it with the Niaoduqing Granule(NDG), so as to provide some laboratory data for the clinic application and innovation of the dosage forms. METHOD: Diuretic effect of the NDT on experimental rats burthened with 1% Sodium deoxycholate was observed by using the metabolize cage examination. The changes of whole blood and plasma viscosity in the blood-stasis rat-model were measured with Viscometer-R80. Plasma was separated and fibrinogen measured by using the turbidimetric method. RESULT: Every dose of NDT had the diuretic effect on experiment rats, but only the big and middle dose increasing the urine quantity in 6 hours had the significance. Each dose could reduce the viscosity of whole blood and the fibrinogen in the blood-stasis rat model, and had the superiority to NDG. CONCLUSIONS: NDT has the diuretic effect and can ameliorate the hemorheology in the blood-stasis rat model, which may delay the course of the chronic renal failure (CRF).

[Laboratory study of the yi-fu-ning soft gelatin capsules in treating climacteric syndrome].

OBJECTIVE: To study the therapeutic mechanism of YFN on climacteric syndrome by investigating the effect of Yi-Fu-Ning soft gelatin capsules (YFN), which can nourish the kidney and activate blood, on serum sex hormone levels and hypothalamic monoamine transmitters contents in ovariectomized rats. METHOD: Fifty female mature Sprague-Dawley rats were randomly divided into 5 groups:sham operation;ovariectomy(OVX);OVX with diethylstilbestrol tablets(DT);OVX with YFN(high dose and low dose). After drugs had been given for 4 weeks, hypothalamic monoamine transmitters (NE, DA, 5-HT, 5-HIAA) contents were detected by fluorospectrophotometric method and serum sex hormone by radioimmunoassay. Adrenal gland index, uterus index and thymus index were also determined. RESULT: YFN could obviously improve serum E2 and increase adrenal gland and uterus index in OVX rats (P < 0.01 or P < 0.05). It could reduce hypothalamic 5-HT and 5-HIAA, which were increased in OVX rats(P < 0.01); It could also increase reduced NE and DA in OVX rats and reduce the ratio of 5-HT to NE and 5-HT to DA(P < 0.01). CONCLUSION: YFN can regulate procreate endocrine in various ways and ameliorate the function of hypothalamic monoamine neurotransmitter in OVX rats. So it can stabilize inner condition of body and relieve symptoms of climacteric syndrome.

Ethyl Acetate Extract from Celastrus aculeatus Merr. Suppresses Synovial Inflammation in Adjuvant Arthritis Rats through Apoptosis Induction of CD4(+)CD25(+)FOXP3(+) T Cells.

Celastrus aculeatus Merr. has been widely used in traditional Chinese medicine to treat rheumatoid arthritis (RA) in clinic. However, the main active fraction of this plant is still unclear. In this study, we attempted to evaluate the suppressive effect of ethyl acetate extract (EAE) from Celastrus aculeatus Merr. on synovial inflammation in adjuvant arthritis (AA) rats induced by Mycobacterium tuberculosis H37Ra (Mtb) and to explore the underlying mechanisms. SD rats immunized with heat-killed Mtb were fed with EAE and observed for erythema, swelling, and induration of each paw. The pathologic changes in joint synovium were tested by hematoxylin-eosin staining. Apoptosis induction of synoviocytes was tested immunohistochemically. Apoptosis of peripheral lymphocytes and the level of regulatory T cells were analyzed by flow cytometry. After treatment with EAE, the joint inflammation in rats with AA was alleviated. Both apoptotic ratios of synoviocytes and peripheral lymphocytes and the ratio of CD4(+)CD25(+)FOXP3(+) to CD4 regulatory T cells were significantly increased. In summary, we first demonstrated that EAE of Celastrus aculeatus Merr. can inhibit synovial inflammation in AA rats through apoptosis induction of CD4(+)CD25(+)FOXP3(+) T cells. Our study provides a rationale for the application of Celastrus aculeatus Merr. to treat RA.

Xiao Yao San Improves Depressive-Like Behaviors in Rats with Chronic Immobilization Stress through Modulation of Locus Coeruleus-Norepinephrine System.

Most research focuses on the hypothalamic-pituitary-adrenal (HPA) axis, hypothalamus-pituitary-thyroid (HPT) axis, and hypothalamus-pituitary-gonadal (HPGA) axis systems of abnormalities of emotions and behaviors induced by stress, while no studies of Chinese herbal medicine such as Xiao Yao San (XYS) on the mechanisms of locus coeruleus-norepinephrine (LC-NE) system have been reported. Therefore, experiments were carried out to observe mechanism of LC-NE system in response to chronic immobilization stress (CIS) and explore the antidepressant effect of XYS. Rat model was established by CIS. LC morphology in rat was conducted. The serum norepinephrine (NE) concentrations and NE biosynthesis such as tyrosine hydroxylase (TH), dopamine-ß-hydroxylase (DBH), and corticotrophin-releasing-factor (CRF) in LC were determined. Results showed that there were no discernible alterations in LC in rats. The serum NE concentrations, positive neurons, mean optical density (MOD), and protein levels of TH, DBH, and CRF in model group were significantly increased compared to the control group. But XYS-treated group displayed a significantly decreased in NE levels and expressions of TH, DBH, and CRF compared to the model group. In conclusion, CIS can activate LC-NE system to release NE and then result in a significant decrease in rats. XYS treatment can effectively improve depressive-like behaviors in rats through inhibition of LC-NE neurons activity.