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1.
Exp Ther Med ; 27(4): 131, 2024 Apr.
Article in English | MEDLINE | ID: mdl-38414788

ABSTRACT

Melasma is an acquired pigmentation disease that mainly involves the development of symmetrical yellow-brown facial patches. The incidence rate of the disease is increasing yearly. Therefore, actively studying the exposure factors that induce melasma could contribute to the prevention and treatment of this disease. In the present review, the possible exposure factors were summarized.

2.
Spectrochim Acta A Mol Biomol Spectrosc ; 280: 121571, 2022 Nov 05.
Article in English | MEDLINE | ID: mdl-35780760

ABSTRACT

A facile and simple colorimetric biosensor was first established for paraquat (PQ) detection based on the aptamer-enhanced oxidation process of 3,3',5,5'-tetramethylbenzidine (TMB) by Ag+. The study confirmed that the interaction of PQ-15 aptamer with Ag+ accelerates the electron transfer from the aptamer-Ag+ complex to dissolved oxygen, which enhances the release of superoxide anion radicals (O2̇-) and facilitates the catalytic oxidation of the chromogenic substrate. PQ-15 aptamer will preferentially bind to PQ molecules, resulting in no further enhancement of the catalytic activity of Ag+. Molecular docking results revealed that the PQ molecules are attached to the stem-loop region of the PQ-15 aptamer through σ-π conjugation interactions. The proposed method is simple that only contains Ag+ and corresponding aptamer. The limit of detection (LOD) of the constructed colorimetric biosensor for PQ detection was determined to be 16.5 µg·L-1, belowing the maximum residue limit in fruits and vegetables set by the EU. Moreover, the colorimetric biosensor showed excellent selectivity and anti-interference properties, which was validated for detecting PQ residues in several typical agricultural and water samples.


Subject(s)
Biosensing Techniques , Metal Nanoparticles , Biosensing Techniques/methods , Colorimetry/methods , Limit of Detection , Metal Nanoparticles/chemistry , Molecular Docking Simulation , Oligonucleotides , Paraquat
3.
J Neural Transm (Vienna) ; 129(5-6): 715-721, 2022 06.
Article in English | MEDLINE | ID: mdl-35190910

ABSTRACT

The first class of site-activated chelators with dual inhibition of acetyl-cholinesterase (AChE) and monoamine oxidase (MAO), rationally designed for simultaneously targeting the multiple pathogenic processes in Alzheimer's disease (AD) without significantly disrupting healthy metal metabolism in the body are discussed. It is demonstrated that the novel prochelator 2 was a selective and potent MAO-A inhibitor in vitro (IC50: 0.0077 ± 0.0007 µM) with moderate inhibition of MAO-B (IC50: 7.90 ± 1.34 µM). In vitro prochelator 2 also selectively inhibited AChE in a time-dependent manner and reach maximum inhibition of AChE after 2 h preincubation (IC50: 0.52 ± 0.07 µM for AChE, versus 44.90 ± 6.10 µM for BuChE). Prochelator 2 showed little affinity for metal (Fe, Cu, and Zn) ions until it bound to and was activated by AChE that is located predominately in the brain, releasing an active iron chelator M30. M30 is an efficient chelator for metal (Fe, Cu, and Zn) ions with the capabilities to suppress oxidative stress, to selectively inhibit MAO-A and B in the brain, and to regulate cerebral biometals dyshomeostasis in vivo; M30 is also a neuroprotective-neurorestorative chelator with a broad spectrum of activities against ß-amyloid (Aß) generation, amyloid plaques and neurofibrillary tangles (NFT) formation, and Aß aggregation induced by metal (Cu and Zn) ions. Both M30 and prochelator 2 were not toxic to Human SH-SY5Y neuroblastoma cells at low concentrations, but prochelator 2 shows limited cytotoxicity, at high concentrations. Together, these data suggest that prochelator 2 is a promise lead for simultaneously modulating multiple targets in AD.


Subject(s)
Alzheimer Disease , Neuroblastoma , Acetylcholinesterase/metabolism , Alzheimer Disease/drug therapy , Amyloid beta-Peptides/metabolism , Cholinesterase Inhibitors/pharmacology , Humans , Iron Chelating Agents/pharmacology , Metals , Monoamine Oxidase/metabolism , Monoamine Oxidase Inhibitors/pharmacology
4.
J Food Biochem ; 46(1): e14000, 2022 01.
Article in English | MEDLINE | ID: mdl-34825388

ABSTRACT

The purpose of this study was to analyze the chemical characterization of Tianshan green tea polysaccharides (TSPS), and evaluate its antioxidant activity by chemical-based and cellular-based antioxidant models in vitro. The results showed that the TSPS were composed of mannose, ribose, rhamnose, glucuronic acid, galacturonic acid, glucose, galactose, arabinose, and fucose with a molar ratio of 14.5:33.5:10.5:6.5:111.5:22.3:59.5:51: 1.0, and an average molecular weight of 19.49 kDa. TSPS exhibited excellent antioxidant ability to DPPH radical, hydroxyl radical, and ABTS radical, and enhanced the ferric-reducing power (FRAP). The antioxidation model of LO2 and HepG2 cells was established, and found that TSPS had no significant toxicity to either of the two cells at the range of 0.1-5 mg/mL, but clearly protected cells from H2 O2 -induced apoptosis and significantly reduced intracellular ROS level. In addition, the activities of antioxidant-associated enzymes were detected in LO2 cells, which suggested that TSPS could significantly improve the activities of SOD and CAT enzyme when the concentration was higher than 0.5 mg/mL. Furthermore, TSPS activated the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway by promoting Nrf2 nuclear translocation and inhibited the expression of Kelch-like ECH-associated protein 1 (Keap-1) and enhanced the expression of heme oxygenase-1 (HO-1). PRACTICAL APPLICATIONS: Tianshan green tea, a local variety in Fujian Province, belongs to unfermented tea. Polysaccharide is considered as the most promising component in Tianshan green tea. This study showed that TSPS had excellent antioxidant activity and had no significant toxicity to cells, which provides a scientific foundation and new idea for its further development and application in functional foods.


Subject(s)
Polysaccharides , Tea , Antioxidants/chemistry , Antioxidants/pharmacology , Oxidation-Reduction , Oxidative Stress , Polysaccharides/chemistry , Polysaccharides/pharmacology , Tea/chemistry
5.
Food Sci Nutr ; 9(9): 4963-4973, 2021 Sep.
Article in English | MEDLINE | ID: mdl-34532008

ABSTRACT

Postharvest melatonin treatments have been reported to improve the quality and storability, especially to inhibit browning in many fruits, but the effect had not been systematically investigated on longan fruit. In this study, the effect of 0.4 mM melatonin (MLT) dipping on the quality and pericarp browning of longan fruits stored at low temperature was investigated. The MLT treatment did not influence the TSS content of longan fruits but lead to increased lightness and h° value while decreased a* value of pericarp. More importantly, the treatment significantly delayed the increase in electrolyte leakage and malonaldehyde accumulation, inhibited the activities of polyphenol oxidase and peroxidase, and thus retarded pericarp browning. In addition, the treatment significantly inhibited the production of O2 •- and H2O2 while promoted the accumulation of glutathione, flavonoids, and phenolics at earlier storage stages in longan pericarp. Interestingly, the activities of ascorbate peroxidase (APX) and superoxide dismutase (SOD) were significantly upregulated but activities of catalase were downregulated in the MLT-treated longan pericarp. MLT treatment effectively enhanced APX and SOD activities, increased flavonoid, phenolics, and glutathione content, protected cytomembrane integrity, inhibited the production of O2 •- and H2O2 and browning-related enzymes, and thus delayed the longan pericarp browning.

6.
Exp Ther Med ; 19(5): 3362-3368, 2020 May.
Article in English | MEDLINE | ID: mdl-32266034

ABSTRACT

The current study investigated the protective effects of inactivated pseudomonas aeruginosa (IPA) on myocardial ischemia reperfusion injury (MIR/I) and the mechanisms governing this interaction. Left anterior descending coronary artery ligation was performed on rats for 30 min and reperfusion was performed for a subsequent 2 h. Rat hearts were obtained and the myocardial infarction area was determined using nitroblue tetrazolium. Myocardial cell apoptosis was determined using flow cytometry. Malondialdehyde (MDA) content, lactate dehydrogenase (LDH) activity, superoxide dismutase (SOD) activity and catalase (CAT) activities were assayed using the corresponding kits. Additionally, nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1) were assayed using western blot and immunofluorescence analysis. When compared with the model group, the results of IPA treatment revealed improved heart function, reduced myocardial infarction area and reduced endothelial cell apoptosis, which led to decreased LDH and MDA levels, and increased SOD and CAT levels in serum, and decreased LDH and MDA levels and increased SOD and CAT in myocardial tissues. Moreover, increased Nrf2 and HO-1 expression levels in the myocardial tissues were also observed at all concentrations of IPA. It was concluded that IPA pretreatment ameliorated MIR/I and reduced endothelial apoptosis and oxidative stress via the Nrf2/HO-1 pathway.

7.
Antioxidants (Basel) ; 9(3)2020 Mar 19.
Article in English | MEDLINE | ID: mdl-32204376

ABSTRACT

In this article, we review how acupuncture regulates oxidative stress to prevent ischemia-reperfusion injury. We electronically searched databases, including PubMed, Clinical Key and the Cochrane Library, from their inception to November 2019 by using the following medical subject headings and keywords: acupuncture, ischemia-reperfusion injury, oxidative stress, reactive oxygen species, and antioxidants. We concluded that acupuncture is effective in treating oxidation after ischemia-reperfusion injury. In addition to increasing the activity of antioxidant enzymes and downregulating the generation of reactive oxygen species (ROS), acupuncture also repairs the DNA, lipids, and proteins attacked by ROS and mediates downstream of the ROS pathway to apoptosis.

8.
BMC Ophthalmol ; 20(1): 105, 2020 Mar 16.
Article in English | MEDLINE | ID: mdl-32178637

ABSTRACT

BACKGROUND: To study the morphologic and biochemical changes in the retina and sclera induced by form deprivation high myopia (FDHM) in guinea pigs and explore the possible mechanisms of FDHM formation. METHODS: Forty 3-week-old guinea pigs were randomized into the blank control (Group I, 20 cases) and model groups (20 cases). In the model group, the right eyes of the guinea pigs were sutured for 8 weeks to induce FDHM (Group II) and the left eyes were considered a self-control group (Group III). The refractive errors were measured with retinoscopy. The anterior chamber depth (AC), lens thickness (L), vitreous chamber depth (V) and axial length (AL) were measured using ultrasonometry A. Retinal and scleral morphology and ultrastructural features were observed with light and electron microscopy. The malondialdehyde (MDA) content and superoxide dismutase (SOD) activity in the retina and sclera were detected with a chemical colorimetric assay. RESULTS: After 8 weeks of stitching, the refractive errors of Group II changed from (+ 3.59 ± 0.33) D to (- 7.96 ± 0.55) D, and these values were significantly higher than those of Group I (+ 0.89 ± 0.32) D and Group III (- 0.55 ± 0.49) D (P < 0.05). The vitreous chamber depth (4.12 ± 0.13) mm and axial length (8.93 ± 0.22) mm of Group II were significantly longer than those of Group I [(3.71 ± 0.23) mm and (7.95 ± 0.37) mm, respectively] and Group III [(3.93 ± 0.04) mm and (8.01 ± 0.15) mm, respectively] (P < 0.05). With the prolongation of form deprivation (FD), the retina and scleral tissues showed thinning, the ganglion cell and inner and outer nuclear layers of the retina became decreased, and the arrangement was disordered. In Group II, the SOD activity was significantly lower than that in Group I and Group III; the MDA content was significantly higher than that in Group I and Group III. The differences were statistically significant (P < 0.05). CONCLUSIONS: These findings suggested that in the FDHM guinea pigs model, the refractive errors, the vitreous chamber depth, and axial length increased significantly with prolongation of monocular FD time, and morphological structural changes in the retina and sclera were observed. Oxygen free radicals might participate in the formation of FDHM.


Subject(s)
Eye Proteins/metabolism , Myopia, Degenerative/diagnosis , Retina/pathology , Sclera/pathology , Animals , Disease Models, Animal , Guinea Pigs , Myopia, Degenerative/metabolism , Retina/metabolism , Retinoscopy , Sclera/metabolism
9.
Biol Trace Elem Res ; 194(1): 203-209, 2020 Mar.
Article in English | MEDLINE | ID: mdl-31172426

ABSTRACT

Zinc (Zn) is an essential trace element for animals. Zn controls the action of more than 300 enzymes and plays an important role in the regulation of gene expression. Evidence has shown that Zn has an antioxidant function, and oxidative damage can occur with Zn deficiency. To assess the effect of Zn deficiency-induced spleen fibrosis, Zn-deficient mice, normal mice, and high-Zn mice were generated and assessed. The Zn content of the spleen in each group was determined, and histopathological examination of the spleens of each group was performed. In the film, we found that the spleens of the Zn-deficient group had high levels of proteinaceous material exudation, interstitial broadening, and lymphocyte reduction, with increased collagen, α-SMA expression, antioxidants, and oxygen free radicals. Zn deficiency inhibited the expression of antioxidants in mice, and the activity of oxygen free radicals in Zn-deficient mice was increased. The detection of α-SMA, collagen 1, and TGF-ß by fluorescence quantitative PCR revealed that the expression index increased in Zn-deficient mice. In addition, to verify the effect of Zn deficiency on the extracellular matrix (ECM) regulatory system, MMPs were determined by real-time PCR, and the expression in the Zn deficiency group was lower than that in the normal group and high-Zn group. The MMP-2 and MMP-13 analyses showed that the expression of the high-Zn group was significantly higher than that of the normal group, indicating that Zn plays an important role in its expression. The above experimental analysis showed that Zn deficiency induces oxygen free radical damage, which further leads to spleen fibrosis.


Subject(s)
Antioxidants/pharmacology , Fibrosis/drug therapy , Spleen/drug effects , Zinc/pharmacology , Animals , Antioxidants/analysis , Fibrosis/metabolism , Fibrosis/pathology , Mice , Oxidative Stress/drug effects , Spleen/metabolism , Spleen/pathology , Zinc/analysis , Zinc/deficiency
10.
Drug Des Devel Ther ; 13: 2827-2832, 2019.
Article in English | MEDLINE | ID: mdl-31496659

ABSTRACT

OBJECTIVE: Tiopronin is an antioxidant. This study investigated the protective effect of tiopronin on oxidative stress in patients with severe burns. METHOD: Patients aged between 16 and 65 years old with >30% body surface area burns admitted to our burn unit from July 2011 to September 2016 were randomly divided into 3 groups: group A treated with tiopronin (15 mg/kg. 24 hrs), group B with vitamin C (792 mg/kg. 24 hrs), the other group with standard treatment (group C). All 3 groups also received standard treatment. Blood superoxide dismutase (SOD), malondialdehyde (MDA), and the biochemical indexes of liver, kidney, and heart were determined before treatment and 24 and 48 hrs after treatment. Samples from 8 normal healthy adult volunteers were also measured. The resuscitation fluid volume requirement for the first 24 hrs was calculated for 3 groups. RESULTS: The serum levels of MDA and the biochemical indexes in severely burned patients were higher than those in healthy volunteers (P<0.01). The serum SOD level of burn patients was lower (P<0.01). After treatment, the levels of SOD increased, the levels of MDA decreased, and the biochemical indexes of heart, liver, and kidney improved; these changes were more obvious in group A and group B compared to group C (P<0.05), and these changes were more obvious in group A compared to group B (P<0.05) at 48 hrs after treatment. There is less resuscitation fluid volume requirement to maintain adequate stable hemodynamic and urine output in the first 24 hrs in group A and group B compared to group C (P<0.05). CONCLUSION: Treatment with tiopronin could exert protective effects against burn-induced oxidative tissue damage and multiple-organ dysfunction, and also could reduce the volume of required fluid resuscitation in severely burned patients.


Subject(s)
Burns/drug therapy , Oxidative Stress/drug effects , Protective Agents/pharmacology , Tiopronin/pharmacology , Adolescent , Adult , Aged , Burns/blood , Dose-Response Relationship, Drug , Female , Humans , Injections, Intravenous , Male , Middle Aged , Protective Agents/administration & dosage , Severity of Illness Index , Tiopronin/administration & dosage , Young Adult
11.
J Cancer Res Ther ; 14(Supplement): S1183-S1187, 2018 Dec.
Article in English | MEDLINE | ID: mdl-30539868

ABSTRACT

AIMS: Breast cancer is a great public health problem. It remains unclear how pharmorubicin induces cardiac dysfunction in patients with breast cancer. Our study was aimed to explore the influence of pharmorubicin on the left ventricular ejection fraction (EF) of patients with breast cancer and its potential mechanism. MATERIALS AND METHODS: Patients with breast cancer were enrolled at the same hospital. Group I consisted of 135 samples, who were under treatment of pharmorubicin (200 mg/m2). Group II consisted of 144 samples, who were under treatment the of pharmorubicin (360 mg/m2). Group III was used as control group, which consists of 120 samples without treatment of pharmorubicin. Color Doppler ultrasonic inspection and measurement were performed to examine EF. Flow cytometry was performed to assess oxygen free radical level in hemocytes. Further combination therapy (N-acetylcysteine [NAC] + pharmorubicin) was provided for patients, and the same examinations were performed for the assessment of cardiac function and oxygen free radical level. RESULTS: The ultrasound results showed that pharmorubicin treatment significantly jeopardized cardiac function, verified by decrease of both EF and fractional shortening (FS) (P < 0. 05). Moreover, such effect was dose-dependent. Oxygen free radical level was remarkably increased after pharmorubicin treatment (P < 0. 05), verified by flow cytometry. Adjunctive therapy of NAC decreased oxygen free radical level and improved cardiac function of patients with breast cancer, suggesting NAC ameliorated side effect of pharmorubicin treatment. CONCLUSIONS: Pharmorubicin treatment decreased EF and FS of patients with breast cancer through increasing oxygen free radical level in hemocytes. Adjunctive therapy of NAC could be a potential treatment to ameliorated side effect pharmorubicin treatment.


Subject(s)
Antibiotics, Antineoplastic/adverse effects , Breast Neoplasms/drug therapy , Epirubicin/adverse effects , Reactive Oxygen Species/blood , Ventricular Dysfunction, Left/blood , Adult , Aged , Echocardiography, Doppler , Female , Humans , Middle Aged , Stroke Volume/drug effects , Ventricular Dysfunction, Left/chemically induced , Ventricular Dysfunction, Left/diagnostic imaging , Ventricular Function, Left/drug effects
12.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-698275

ABSTRACT

Objective To observe the curative effect of Fuzhengxiaojia decoction on precancerous lesion of gastric cancer (PLGC).Methods We randomly divided 44 patients with PLGC in our hospital into control group (n=22)and treatment group (n=22).The control group was given 4 Weifuchun tablets each time and three times per day and while the treatment group was given one Fuzhengxiaojia decoction of 400 mL besides the medication of the control group.They were treated for two courses,one course lasting for one month.Results Superoxide dismutase (SOD),malondialdehyde (MDA),glutathione peroxidase (GSH-Px),IgG,IgM and IgA in the two groups had no significant differences before treatment (P>0.05).After treatment,compared with those in the control group,SOD (t=2.144,P=0.044)and GSH-Px (t=2.322,P=0.030)increased,while MDA(t=3.096, P=0.005),IgG(t=2.421,P=0.025),IgM(t=3.377,P=0.003)and IgA (t=2.521,P=0.020)decreased. The main symptom scores in the two groups did not significantly differ before treatment (P<0.05).After treatment, compared with those in the control group,the scores for main symptoms like reduced food intake (t=3.924,P<0.001),stomach noise (t=4.161,P<0.001)and gastric or hypochondriac swelling (t=2.881,P<0.009) decreased in the treatment group.The rate of effective cases was higher than that in the control group (χ2=4.539, P=0.033).Conclusion The effect of Weifuchun combined with Fuzhengxiaojia prescriptions in treating PLGC is better than Weifuchun alone,which is related to improving redox and immunoglobulin.

13.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-692530

ABSTRACT

Objective To study the preventive effect of epigallocatechin gallate(EGCG)on hyperoxiainduced bronchopulmonary dysplasia in mice.Methods Eighty-eight Kunming mice born 36-40 hours were randomly divided into four groups:air + saline group (n =22),air + EGCG group (n =22),hyperoxia + saline group(n =22) and hyperoxia + EGCG group(n =22).Drug was administrated once a day by air-driven atomization,till 28 days.Furthermore,the hyperoxia groups were transferred into the room air for recovery after raised in (70 ± 3) % oxygen for 28 days.Lung pathological morphology and homogenization ELISA were performed on the 21th,28th and 49th day.The pathological changes of lung tissue radical alveolar counts(RAC) were observed and the levels of interleukin-2 (IL-2),tumor necrosis factor(TNF-α) and myeloperoxidase(MPO) were measured.Results The levels of IL-2 and TNF-α in the air groups were significantly lower than those in hyperoxia group(IL-2:air(1 760.83 ±303.38)pg/g vs hyperoxia(4 251.00 ±644.07) pg/g;TNF-a:air(4 308.83 ±1 114.91) pg/g vs hyperoxia(8301.83 ± 802.26) pg/g) (P < 0.01),and MPO level decreased in hyperoxia +EG-CG group(7 472.83 ± 1 922)U/g,hyperoxia +NS group(4 767.68 ± 1 110.72)U/g,air + EGCG group(3712.68 ± 734.40)U/g,air + NS group(2 711.68 ± 763.39)U/g(P <0.05).In the hyperoxia groups,though IL-2 on 21th day and TNF-αt on 49th day were no statistic difference in hyperoxia group and air group,the inflammatory factors in EGCG group were lower than in hyperoxia + NS group.Pathology showed that the RAC count of the air groups increased gradually,while the hyperoxic groups were gradually decreased,however,the EGCG group tend to recover after 21 days recovery in room air.Conclusion Inhalation of EGCG can reduce the level of inflammatory response in lung tissue of hyperoxia exposed mice.EGCG attenuated lung injury in hyperoxia-exposed mice,and accelerated lung recovery after hyperoxia exposure in experimental animals.EGCG has potential effect to prevent hyperoxia induced bronchopulmonary dysplasia.

14.
Biosci Rep ; 37(6)2017 Dec 22.
Article in English | MEDLINE | ID: mdl-29026009

ABSTRACT

Although restoration of blood flow to an ischemic organ is essential to prevent irreversible cellular injury, reperfusion may augment tissue injury in excess of that produced by ischemia alone. So this experiment was designed to study the protective effects and mechanism of inactivated Lactobacillus (Lac) on myocardial ischemia-reperfusion (I-R) injury (MIRI). MIRI rat models were established by ligation of left anterior descending coronary artery for ~30 min and then, reperfusion for 120 min and divided into control group, model group, and Lac (106, 107, and 108 cfu/kg) groups. At the end of the test, the creatine kinase (CK) activity, lactate dehydrogenase (LDH) activity, superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were assayed by corresponding kits. The heart was obtained from rats and the myocardial infarction area was determined by TTC staining and myocardial endothelial cell apoptosis rate was determined by Tunel kit. Besides, A20, IκB, nuclear factor (NF)-κB, and nitric oxide (NO) synthase (NOS) were also assayed by Western blot. When compared with model group, Lac obviously reduces MIRI in the rat by reducing myocardial infarction area and the apoptosis rate of endothelial cells; reduce the serum CK, LDH, and MDA content; increase the serum SOD activity; and suppress NF-κB signaling and NOS expression in the myocardial tissues. Lac pretreatment can inhibit lipid peroxidation and effectively improve MIRI caused by oxygen free radical through inhibiting NF-κB signaling.


Subject(s)
Lactobacillus/physiology , Myocardial Infarction/physiopathology , Myocardial Reperfusion Injury/prevention & control , Myocardium/metabolism , NF-kappa B/metabolism , Animals , Apoptosis , Disease Models, Animal , Female , Male , Metabolic Networks and Pathways , Myocardial Reperfusion Injury/metabolism , Myocardium/pathology , Nitric Oxide Synthase/metabolism , Rats , Rats, Sprague-Dawley
15.
The Journal of Practical Medicine ; (24): 3012-3016, 2017.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-658454

ABSTRACT

Objective To investigate the expression of dopamine receptor in brain of rats with pancreatic encephalopathy and provide a theoretical basis to reveal pathogenesis of pancreatic encephalopathy. Methods A rat model of experimental pancreatic encephalopathy was induced by retrograde injection of 5%sodium taurocholate into the pancreatic duct. The pathological changes of pancreas and brain were detected. The water content in brain tissue was determined. The superoxide dismutase activity and malondialdehyde content in brain tissue homogenate were detected by the chemical colorimetry. Levels of TNF-α,IL-1β,tyrosine hydroxylase and dopamine receptor-2 were detected by immunohistochemistry(SP method). Results Cerebral sulcus was shallow,ventricle was small-er and the superficial veins were dilated and congested. The inflammatory cell infiltration and pancreatic acinar cell necrosis in the pancreas and neuron edema ,inflammatory cell infiltration ,microvessel adherent leukocytes in brain were observed by light microscope in model groups at 3,6,12 hours. Compared with the control group. The activities of superoxide dismutase in brain tissue in model groups at 3,6,12 hours were significantly decreased (P < 0.01). The level of malondialdehyde and the water content of brain tissue were significantly increased (P <0.01 ,respectively). Compared with the control group ,levels of brain TNF-α,IL-1β,tyrosine hydroxylase and dopamine receptor-2 in model groups at 3,6,12 hours were significantly increased(P < 0.01,respectively).Conclusions The incidence of pancreatic encephalopathy may be related to the influx of oxygen free radical and inflammatory factors,invading nerve center by blood-brain barrier and inducing the increased production of dopa-mine and the upregulation of dopamine receptor in brain.

16.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-616059

ABSTRACT

Long non-coding RNA plays an increasingly important role in transcriptional, post-transcriptional and epigenetic levels. In ischemic heart disease, most studies on long non-coding RNA focused on myocardial infarction, hypertrophy and fibrosis, and a few of reports directly focused on the pathological process of myocardial reperfusion injury. Thus, the purpose of this review is to introduce the processes of long non-coding RNA in myocardial reperfusion injury field, aiming to provide a novel research and theraputic method for exploring the mechanism and molecular regulation network involed with reperfusion injury.

17.
Journal of Medical Postgraduates ; (12): 926-931, 2017.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-613044

ABSTRACT

Objective To investigate the mechanisms of oxygen free radical/JNK signaling pathway on neuronal autophagy after subarachnoid hemorrhage(SAH) in rats.Methods 160 male Sprague-Dawley rats were randomly divided into four groups: sham group, SAH model group, low dose Edaravone group and high dose Edaravone group.The SAH model was established by autologous blood injection into cisterna magna twice, while the rats in the sham group were injected with isotonic saline(0.3mL/time).The high dose of edaravone group and low dose of edaravone group were given 5mg/kg or 10mg/kg of edaravone, respectively, once daily with tail intravenous injection after the models were established.The morphological changes of hippocampus neural cells were detected by light microscope.The malondialdehyde (MDA) level in brain tissue was determined with thiobarbituric acid.The changes of phosphorylated JNK and autophagic biomarkers (Beclin-1 and LC3-II)were detected by immunohistochemical method.The expressions of JNK mRNA,Beclin-1 mRNA and LC3 mRNA in hippocampus was detected by Real time-quantitative PCR.Results The necrotic nerve cells were seen in the hippocampus of SAH group in terms of nuclear dissolution, nuclear fragmentation or nuclear disappearance.Compared with Sham group, the level of MDA and the number of dead neurons, the expression of JNK mRNA, Beclin-1 mRNA and LC3-Ⅱ mRNA were increased in the SAH group (P<0.05).The survival rate of nerve cells in the SAH group was lower than that in the sham group.The immunoreactivity of phosphorylated JNK 、Beclin-1 and LC3-Ⅱ in the SAH group was enhanced than that in the sham group.However the damage of the morphological structure of nerve cells was relatively decreased in both doses groups.Compared with SAH group, the level of MDA and the expression of JNK mRNA in low dose Edaravone group and high dose Edaravone group were decreased.The expression of Beclin-1 mRNA and LC-3 mRNA was higher (P<0.05).Furthermore, the survival rates of nerve cells in both dosesgroups were higher than that in the SAH group (P<0.05).Meanwhile, the immunoreactivity of phosphorylated JNK in both doses groups was weakened than that in the SAH group.The mRNA expression of Beclin-1 and LC3-Ⅱ was increased(P<0.05).Conclusion Oxygen free radical played an important role in process of neuronloss by activating the JNK signaling pathway to regulate Beclin-1 and LC3-Ⅱ expression.

18.
Clinical Medicine of China ; (12): 1010-1013, 2017.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-663916

ABSTRACT

Objective To investigate the effects of combination of tandospirone,mosapride and Bella ray on the levels of oxygen free radicals and inflammatory cytokines in patients with reflux esophagitis.Methods From March 2016 to March 2017,ninety cases with reflux esophagitis treated in Nanchong Central Hospital were involved in this study.The patients were divided into the observation group and the control group according to different treatment methods,45 cases in each group.Patients in the observation group were treated with tandospirone and mosapride combined with ray Bella with treatment,patients in the control group were treated with Mosapride combined with Bella ray,the therapeutic effect of two groups were observed and compared,oxygen free radical and inflammatory cytokines before and after treatment of the two groups were compared.Results After treatment,MDA and AOPP of the patients in the observation group were(16.51±2.6)U/L and(36.5 ±4.5)μmol/L,significantly lower than those in the control group(MDA:(20.8±2.9)U/L,AOPP:(59.9 ±4.8)mol/L).Glutathione peroxidase(GSH-PX)and superoxide dismutase(SOD)in the observation group were significantly higher than those in the control group((249.4 ± 32.3)mg/L vs.(228.6 ± 17.2)mg/L, (27.3± 3.4)mg/L vs.(18.8 ± 2.7)mg/L),the differences were statistically significant(t=33.5,32.3, 31.4.32.7,P<0.05).After treatment,the levels of TNF-a,IL-6,IL-8 were significantly lower than those in the control group(17.7±2.8)μg/L vs.(26.3±1.5)μg/L,(4.9±0.3)ng/L vs.(6.5±1.8)ng/L,(5.4±0.7) μg/L vs.(6.6±0.8)μg/L),the differences were statistically significant(t=36.3,31.5,32.4,P<0.05).In the observation group,22 cases were significantly effective,19 cases were effective and 4 cases were ineffective, the effective rate was 91.1%,which was significantly higher than that of the control group(86.7%),(χ2=29.5,P=0.02).Conclusion Tandospirone combined with Bella ray can reduce the levels of oxygen free radicals and inflammatory cytokines in patients with reflux esophagitis.

19.
The Journal of Practical Medicine ; (24): 3012-3016, 2017.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-661373

ABSTRACT

Objective To investigate the expression of dopamine receptor in brain of rats with pancreatic encephalopathy and provide a theoretical basis to reveal pathogenesis of pancreatic encephalopathy. Methods A rat model of experimental pancreatic encephalopathy was induced by retrograde injection of 5%sodium taurocholate into the pancreatic duct. The pathological changes of pancreas and brain were detected. The water content in brain tissue was determined. The superoxide dismutase activity and malondialdehyde content in brain tissue homogenate were detected by the chemical colorimetry. Levels of TNF-α,IL-1β,tyrosine hydroxylase and dopamine receptor-2 were detected by immunohistochemistry(SP method). Results Cerebral sulcus was shallow,ventricle was small-er and the superficial veins were dilated and congested. The inflammatory cell infiltration and pancreatic acinar cell necrosis in the pancreas and neuron edema ,inflammatory cell infiltration ,microvessel adherent leukocytes in brain were observed by light microscope in model groups at 3,6,12 hours. Compared with the control group. The activities of superoxide dismutase in brain tissue in model groups at 3,6,12 hours were significantly decreased (P < 0.01). The level of malondialdehyde and the water content of brain tissue were significantly increased (P <0.01 ,respectively). Compared with the control group ,levels of brain TNF-α,IL-1β,tyrosine hydroxylase and dopamine receptor-2 in model groups at 3,6,12 hours were significantly increased(P < 0.01,respectively).Conclusions The incidence of pancreatic encephalopathy may be related to the influx of oxygen free radical and inflammatory factors,invading nerve center by blood-brain barrier and inducing the increased production of dopa-mine and the upregulation of dopamine receptor in brain.

20.
Herald of Medicine ; (12): 473-476, 2017.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-512346

ABSTRACT

Objective To investigate the effect and the potential mechanisms of low molecular polysaccharide from agaricus blazei (LMPAB) on H2O2-induced oxidative injury in hippocampal neuronal cells of rats.Methods Hippocampal neuronal cells were isolated from SD rats (24 h) and grew in culture.Cultured cells were divided into normal control group (added the same amount of nutrient solution), model control group (added 500 μmol·L-1H2O2 solution) and LMPAB high, medium, low dose groups (added 20,10,5 mg·L-1 LMPAB solution, respectively, then added 500 μmol·L-1 H2O2 solution each).The hippocampal neuron cell activity was detected with MTT method.The hippocampus neuron mitochondrial membrane potential (MMP) was detected by flow cytometry.According to the reagent instruction methods, malondialdehyde (MDA), catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) activities were detected.Results The activities of cell, CAT, SOD, GSH-PX and MMP in normal control group and the LMPAB high dose group were significantly higher than those of model control group (P<0.01);The content of MDA in normal control group and LMPAB high dose group was significantly lower than that of model control group (P<0.01).Conclusion The protective effect of LMPAB on hippocampal neurons with H2O2-induced injury may be related with the mechanism of enhancing the neuronal antioxidative capacity.

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