#( LDH ; int )

[ramenarchived]

Es consiente que si sus compañeros de trabajo se enteraban que había si quiera entrado en aquel local lo molestarían por, en su punto de vista, cometer traición, pero Dae solo aprovechaba el tener una cafetería enfrente de la universidad y los cupones que regalaban a los estudiantes. Siendo estos la razón por la que ahora contaba con una bebida extra.

“Hey, ¿quieres un café gratis?” preguntó a la persona atrás de él en la fila.

[ddarchive]

[ New message ]

Dae: Cambio de planes, mis servicios de niñero han sido solicitados y no podre asistir a lo de esta noche. Avísame si algo ocurre.

[ramenarchived]

xlittleprinccss​:

          ❝——No estoy segura que desee saber❞ pero claramente notaba la sangre y parecía que sin duda había sido algo muy malo, lo que menos necesitaba saber era si eso se trataba de algo ilegal. ❝Eso no suena nada bien…❞ admitió, y no podía evitar tener su mirada en él.  

"Tu preguntaste." Señaló con un encogimiento de hombros, evidentemente a él no le causaba gran preocupación. "¿Acaso no te alegra que no sea mía? ¿Qué no me haya lastimado?" Cuestionó fingiendo que sus palabras le habían herido.

[rnomics]

Long non-coding #RNA MALAT1 functions as a mediator in cardioprotective effects of fentanyl in myocardial ischemia-reperfusion injury.

Related Articles Long non-coding #RNA MALAT1 functions as a mediator in cardioprotective effects of fentanyl in myocardial ischemia-reperfusion injury. Cell Biol Int. 2017 Jan;41(1):62-70 Authors: Zhao ZH, Hao W, Meng QT, Du XB, Lei SQ, Xia ZY Abstract Long non-coding (l#ncRNA) MALAT1 can be increased by hypoxia or ischemic limbs. Also, downregulation of MALAT1 contributes to reduction of cardiomyocyte apoptosis. However, the functional involvement of MALAT1 in myocardial ischemia-reperfusion (I/R) injury has not been defined. This study investigated the functional involvement of l#ncRNA-MALAT1 in cardioprotective effects of fentanyl. HL-1, a cardiac muscle cell line from the AT-1 mouse atrial cardiomyocyte tumor lineage was pre-treated with fentanyl and generated cell model of hypoxia-reoxygenation (H/R). Relative expression of MALAT1, miR-145, and Bnip3 #mRNA in cells was determined by quantitative real-time PCR. Cardiomyocyte H/R injury was indicated by lactate dehydrogenase (LDH) release and cell apoptosis. The results showed that fentanyl abrogates expression of responsive gene for H/R and induces downregulation of MALAT1 and Bnip3 and upregulation of miR-145. We found that miR-145/Bnip3 pathway was negatively regulated by MALAT1 in H/R-HL-1 cell with or without fentanyl treatment. Moreover, both MALAT1 overexpression and miR-145 knockdown reverse cardioprotective effects of fentanyl, as indicated by increase in LDH release and cell apoptosis. The reversal effect of MALAT1 for fentanyl is confirmed in cardiac ischemia/reperfusion (I/R) mice. In summary, l#ncRNA-MALAT1 is sensitive to H/R injury and abrogates cardioprotective effects of Fentanyl by negatively regulating miR-145/Bnip3 pathway. PMID: 27862640 [PubMed - indexed for MEDLINE] http://bit.ly/2iZT9sN #Pubmed

[healthtimetaylor]

Crocetin might halt or delay disease progression in age-related macular degeneration.

PMID:  Int J Mol Sci. 2020 Apr 22 ;21(8). Epub 2020 Apr 22. PMID: 32331354 Abstract Title:  Crocetin Prevents RPE Cells from Oxidative Stress through Protection of Cellular Metabolic Function and Activation of ERK1/2. Abstract:  Age-related macular degeneration (AMD) is a leading cause for visual impairment in aging populations with limited established therapeutic interventions available. Oxidative stress plays an essential role in the pathogenesis of AMD, damaging the retinal pigment epithelium (RPE), which is essential for the function and maintenance of the light-sensing photoreceptors. This study aimed to evaluate the effects of crocetin, one of the main components of Saffron, on an in vitro RPE model of tert-butyl hydroperoxide (TBHP) induced oxidative stress using ARPE19 cells. The effects of crocetin were assessed using lactate de-hydrogenase (LDH) and ATP assays, as well as immunocytochemistry for cell morphology, junctional integrity, and nuclear morphology. The mechanism of crocetin action was determined via assessment of energy production pathways, including mitochondrial respiration and glycolysis in real-time as well as investigation of extracellular signal-regulated kinase 1/2 (ERK1/2) activation and distribution. Our results show that crocetin pre-treatment protects ARPE19 cells from TBHP-induced LDH release, intracellular ATP depletion, nuclear condensation, and disturbance of junctional integrity and cytoskeleton. The protective effect of crocetin is mediated via the preservation of energy production pathways and activation of ERK1/2 in the first minutes of TBHP exposure to potentiate survival pathways. The combined data suggest that a natural antioxidant, such as crocetin, represents a promising candidate to prevent oxidative stress in RPE cells and might halt or delay disease progression in AMD.

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[lopezdorothy70-blog]

Huperzine A ameliorates damage induced by acute myocardial infarction.

PMID:  Int J Mol Med. 2014 Jan ;33(1):227-33. Epub 2013 Nov 1. PMID: 24190328 Abstract Title:  Huperzine A ameliorates damage induced by acute myocardial infarction in rats through antioxidant, anti-apoptotic and anti-inflammatory mechanisms. Abstract:  Huperzine A (HupA), an alkaloid used in traditional Chinese medicine and isolated from Huperzia serrata, has been shown to possess diverse biological activities. The present study was undertaken to evaluate the cardioprotective potential of HupA in myocardial ischemic damage using a rat model of acute myocardial infarction. HupA significantly diminished the infarct size and inhibited the activities of myocardial enzymes, including creatine kinase (CK), the MB isoenzyme of creatine kinase (CK-MB), lactate dehydrogenase (LDH) and cardiac troponin T (cTnT). A significantly reduced activity of malondialdehyde (MDA) and elevated activities of superoxide dismutase (SOD), of the non-enzymatic scavenger enzyme, glutathione (GSH), as well as of glutathione peroxidase (GSH-PX) were found in the HupA-treated groups. Furthermore, decreased protein levels of caspase-3 and Bax, and increased levels of Bcl-2 were observed in the infarcted hearts of the rats treated with various concentrations of HupA. In addition, treatment with HupA markedly inhibited the expression of the nuclear factor-κB (NF-κB) subunit p65, tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). These findings suggest that the cardioprotective potential of HupA is associated with its antioxidant, anti-apoptotic and anti-inflammatory properties in acute myocardial infarction in rats.

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[ramenarchived]

● ◜send ☎ for your muses info in my muses phone◞ ●

( @toxxuki  —  trama: SHN x Dae Hyun ) ♪

[ddarchive]

@kuro-usagi​​ send 💕 from this:: YOUR MUSE TELLING MY MUSE THAT THEY WILL ALWAYS BE FRIENDS

“Sólo dices eso para que te siga llevando a todos lados,” acusó, soltando una carcajada al final, aunque en realidad a su billetera no le parecía nada gracioso. “Los sentimientos no pagan por la gasolina, pequeña.”

[healthtimetaylor]

Krill oil might be a new candidate for treatment of iron overload-induced toxicity.

PMID:  Environ Sci Pollut Res Int. 2020 Feb ;27(4):3950-3961. Epub 2019 Dec 10. PMID: 31823254 Abstract Title:  Krill oil alleviates oxidative stress, iron accumulation and fibrosis in the liver and spleen of iron-overload rats. Abstract:  Krill oil (KO) is a recent supplement which is rich in eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). These fatty acids are found in both krill oil and fish oil. In krill oil, they esterified to phospholipids, but in fish oil, they are esterified to triacylglycerols. The target of this study was to investigate whether KO could help against iron overload-induced toxicity in liver and spleen. Rats were randomly assigned into 3 categories: control rats, rats received iron in a drinking water for 8 weeks followed by either vehicle or KO (40 mg/kg) treatment for an extra 8 weeks. Extent of hepatic and splenic injury was assessed via biochemical, histopathological and immunohistochemical evaluations. KO effectively improved the microscopic features of liver and spleen. Moreover, it decreased the increased levels of serum transaminases, ALP, LDH, iron, and ferritin and increased albumin serum level as well. In addition, it restored the balance between oxidants and antioxidants in the hepatic and splenic tissues. Furthermore, it decreased HO-1 levels, upregulated the production of Nrf2, and limited the expression of MMP9. These findings altogether suggest that KO might be a new candidate for treatment of iron overload-induced toxicity. Graphical abstract Graphical abstract.

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[healthtimetaylor]

Quercetin could be used as a protective agent against BPA-induced mitochondrial toxicity.

PMID:  Environ Sci Pollut Res Int. 2020 Feb 17. Epub 2020 Feb 17. PMID: 32064580 Abstract Title:  Protective effects of quercetin against oxidative stress induced by bisphenol-A in rat cardiac mitochondria. Abstract:  Research has shown a relationship between the exposures to a chemical agent called bisphenol-A (BPA), which is extensively used in the production of polycarbonate plastics and the incidence of cardiovascular diseases. This association is most likely caused by the BPA's ability to disrupt multiple cardiac mechanisms, including mitochondrial functions. Therefore, this study aimed to explore the ability of quercetin (QUER) to limit the cardiotoxic effect of BPA in the rat's cardiac mitochondria. The experiment was carried out on 32 male Wistar rats, which were randomly assigned to four groups. The negative control group received olive oil; the positive control group received olive oil plus BPA (250 mg/kg); the third group received olive oil, BPA, and QUER (75 mg/kg); and the fourth group received olive oil and QUER, all orally for 14 days. The rats were slaughtered 24 h after the last treatment. The measured parameters included creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH) asthe biomarkers of cardiotoxicity, triglyceride (TG), total cholesterol (TC), and low-density and high-density lipoprotein cholesterol (LDL-C and HDL-C) as the measures of dyslipidemia, glutathione (GSH) content, catalase activity (CAT), reactive oxygen species (ROS), lipid peroxidation (LPO), and the level of damage to the mitochondrial membranes as the indicators of the impact of QUER on the BPA cardiotoxic effect. Finally, the rats treated with QUER showed better results in terms of serum CK-MB, serum LDH, serum lipid profile, GSH level, CAT activity, mitochondrial membrane potential (ΔΨm), LPO, and ROS. According to the results, QUER could be used as a protective agent against BPA-induced mitochondrial toxicity.

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[healthtimetaylor]

Chitosan oligosaccharides alleviate particulate matter-induced lung inflammation.

PMID:  Environ Sci Pollut Res Int. 2018 Dec ;25(34):34221-34227. Epub 2018 Oct 5. PMID: 30291606 Abstract Title:  Chitosan oligosaccharides alleviate PM-induced lung inflammation in rats. Abstract:  Air pollution of particulate matter (PM), especially PM, has become a major public health problem in China. Exploration of therapeutic and preventive measures against PMtoxicity is of practical significance. The aim of this study was to examine the inhibitory effects of chitosan oligosaccharides (COS) on PM-induced lung inflammation in rats. Forty SPF (specific pathogen-free) male Wistar rats weighing 200-220 g were randomly divided into four groups: control group, COS group, PMgroup, and PM+COS group. COS was pre-administered to rats by gavage at a single dose of 500 mg/kg 2 h before intratracheal instillation of PMat a single dose of 1.2 mg/kg daily for 3 consecutive days. Normal saline (NS) was used as negative control. Twenty-four hours after the last instillation of PM, rats were sacrificed and subjected to bronchoalveolar lavage (BAL). The BAL fluids (BALF) were collected for measurement of levels of total proteins, lactate dehydrogenase (LDH), interleukin-1 (IL-1β), IL-8, and tumor necrosis factor-ɑ (TNF-ɑ) using colorimetric or ELISA kits. Levels of total proteins, LDH activities, and pro-inflammatory mediators including IL-1β, IL-8, and TNF-ɑ in BALF of rats in PMgroup significantly increased in comparison with those of the control group. Pre-treatment of rats with COS markedly blocked PM-induced increase in LDH, IL-8, and TNF-ɑ levels in BALF. In conclusion, PMexposure induces rat lung inflammation, which could be ameliorated by the pre-treatment of COS.

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[healthtimetaylor]

Short-term Ubiquinol-10 supplementation alleviates tissue damage in muscle and fatigue caused by strenuous exercise in male distance runners.

PMID:  Int J Vitam Nutr Res. 2020 Jan 31:1-10. Epub 2020 Jan 31. PMID: 32003645 Abstract Title:  Short-term Ubiquinol-10 supplementation alleviates tissue damage in muscle and fatigue caused by strenuous exercise in male distance runners. Abstract:  Coenzyme Q10 (CoQ10) is the electron transporter in oxidative phosphorylation and an endogenous antioxidant. Recent researches have indicated that doses of 200-300 mg/day are needed to recognize effects to prevent oxidative damage in athletes, and the reduced form of CoQ10, ubiquinol-10, is more bioavailable than its oxidized form. Therefore, we hypothesized that higher doses of ubiquinol-10 could elevate plasma CoQ10 levels rapidly and exert physiological benefits in athletes. Therefore, a placebo controlled, double blinded test was carried out to determine the effects of ubiquinol-10 on the extravasate enzymes and fatigue levels of distance runners.Sixteen male collegiate distance runners were allocated to two groups receiving 300 mg/day of ubiquinol-10 (19.8 ± 1.7 years) or a placebo (20.1 ± 1.6 years) for 12 days during summer training that comprised 25- and 40-km runs on days 7 and 9, respectively.Ubiquinol-10 elevated plasma CoQ10 concentration to 5.62 μg/mL and significantly decreased activities of the serum extravasate enzymes, CK, ALT, LDH (P 

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[healthtimetaylor]

Oleuropein and hydroxytyrosol-rich olive leaf extracts possessed hypolipidemic and hepatoprotective effects against HFD-induced metabolic disorders.

PMID:  Biomed Res Int. 2020 ;2020:1315202. Epub 2020 Jan 8. PMID: 31998777 Abstract Title:  Comparative Study on Beneficial Effects of Hydroxytyrosol- and Oleuropein-Rich Olive Leaf Extracts on High-Fat Diet-Induced Lipid Metabolism Disturbance and Liver Injury in Rats. Abstract:  Oleuropein and hydroxytyrosol, as major compounds of olive leaves, have been reported to exert numerous pharmacological properties, including anticancer, antidiabetic, and anti-inflammatory activities. The purpose of this study is to evaluate and compare the protective effect of oleuropein- and hydroxytyrosol-rich extracts, derived from olive leaves, on high-fat diet-induced lipid metabolism disturbance and liver injury in rats. In this respect, four groups of male rats (8 per group) were used: control group (Control), group treated with high-fat diet (HFD), group treated with HFD and oleuropein (HFD + OLE), and group treated with HFD and hydroxytyrosol (HFD + HYD). The current research showed that the treatment with the HFD increased the body weight and adipose tissue mass in male rats. Moreover, the plasma levels of triglycerides, total cholesterol, LDL-cholesterol, AST, ALT, LDH, andTNF-were also raised. The hepatic immunohistochemical analysis revealed a significant increase in the expression of inflammatory genes (COX-2, NF-B, and TNF-). Equally, it showed a rise of the apoptotic markers (a decrease in the expression of the Bcl-2 and an increase of the P53). In addition, the oral administration of oleuropein- and hydroxytyrosol-rich olive leaf extracts at 16 mg/kg similarly reduced the body weight and adipose tissue mass and improved the lipid profile. Moreover, these extracts, mainly the hydroxytyrosol-rich extract, reduced the elevated liver enzymes, enhanced the antioxidant status, and attenuated the liver inflammation and apoptosis. These findings suggest that the oleuropein- and hydroxytyrosol-rich olive leaf extracts possessed hypolipidemic and hepatoprotective effects against the HFD-induced metabolic disorders by enhancing the antioxidative defense system and blocking the expression of the proteins involved in inflammation and liver damage.

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[healthtimetaylor]

Vitamin C supplementation had anticancer properties in ovarian cancer cells.

PMID:  Int J Vitam Nutr Res. 2020 Feb 3:1-11. Epub 2020 Feb 3. PMID: 32008465 Abstract Title:  Vitamin C supplementation had no side effect in non-cancer, but had anticancer properties in ovarian cancer cells. Abstract:  Vitamin C (Vit C) has been widely used in the treatment and prevention of cancer. Nevertheless, the clinical results are still inconclusive. Using non-cancer (HOSEpiC) and cancer OVCAR-3 cells cultured in basal medium or in ovarian cancer-associated fibroblast (CAF)-supplemented medium, we estimated the dose-dependent effect of Vit C on sodium-ascorbate coSVCT1, SVCT2) and g(GLUT1) protein expression. Additionally, the action of Vit C on cell proliferation (alamarBlue), membrane permeability (LDH assay), caspase3 activity, the selected cell cycle and apoptosis pathway, poly(ADP-ribose) polymerase-1 (PARP) protein expression, and reactive oxygen species (ROS) activity was determined. We showed different effects of Vit C on the expression of the co-transporter in non-cancer and cancer cells. In non-cancer cells, Vit C, at a pharmacological concentration, increased SVCT2 and decreased GLUT1, while the opposite effect was noted in cancer cells. In cancer cells, Vit C, in a pharmacological dose, decreased cell proliferation through an inhibitory effect on cyclin-dependent kinase 2 (CDK2) (4.4-fold; p 

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[healthtimetaylor]

Hepatoprotective role of berberine against paraquat-induced liver toxicity in rat.

PMID:  Environ Sci Pollut Res Int. 2019 Dec 16. Epub 2019 Dec 16. PMID: 31845254 Abstract Title:  Hepatoprotective role of berberine against paraquat-induced liver toxicity in rat. Abstract:  Paraquat (PQ) is a herbicide agent commonly used in agricultural applications. Hepatotoxicity is among clinical complications associated with PQ intoxication. Oxidative stress and its subsequent events are major mechanisms identified in PQ-induced liver toxicity. Berberine (BBR) is a natural antioxidant widely investigated for its hepatoprotective effects. The present study designed to evaluate the potential cytoprotective properties of BBR against PQ-induced cytotoxicity in primary cultured rat hepatocytes and in vivo test of liver function enzymes. Cellular and biochemical parameters including lactate dehydrogenase (LDH), cell viability, ROS formation, glutathione (GSH) content, and mitochondrial membrane potential in the PQ-treated hepatocytes were measured, and the mentioned markers were evaluated in the presence of BBR. BBR treatment caused significant decrease in PQ-induced cell death, ROS formation, and LDH release. On the other hand, it was found that BBR inhibits cellular glutathione depletion in PQ-treated hepatocytes. Also, BBR treatment significantly diminished PQ-induced the liver function enzyme elevation. These data mention the potential hepatoprotective effect of BBR with therapeutic capability against PQ-induced liver damage.

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[healthtimetaylor]

Protective effects of resveratrol supplementation on contusion induced muscle injury.

PMID:  Int J Med Sci. 2020 ;17(1):53-62. Epub 2020 Jan 1. PMID: 31929738 Abstract Title:  Protective Effects of Resveratrol Supplementation on Contusion Induced Muscle Injury. Abstract:  Muscle injuries frequently occur in contact sports events. The current treatment options for soft tissue injuries remain suboptimal and often result in delayed or incomplete recovery of damaged muscles. Resveratrol (RES) is a phenolic phytochemical, well-known for its antioxidant and anti-inflammatory properties. The purpose of this study is to evaluate the potential beneficial effects of RES supplementation on inflammation and regeneration in skeletal muscle after a contusion injury, in comparison to a conventional treatment of nonsteroidal anti-inflammatory drugs (NSAID). After one week of acclimation, forty eight -week-old male ICR mice were randomly divided into the five groups (n=8 per group): 1) normal control (NC), 2) mass-drop injury without any treatment (mass-drop injury, MDI), 3) post-injury NSAID treatment (MDI+ 10mg/kg NSAID), 4) post-injury RES supplementation (MDI+ 25mg/kg/day RES) and 5) post-injury treatment with RES and NSAID (MDI + resveratrol+ NSAID). After muscle contusion injury of the left gastrocnemius muscle, RES or NSAID were orally administered post-injury once a day for 7 days. Results showed that the MDI group had significantly higher serum uric acid (UA), CREA (creatinine), LDH (lactic dehydrogenase) and creatine kinase (CK) than the normal control group. Treatment with resveratrol reduced muscle damage as evidenced by the significantly decreased serum levels of UA, CREA, LDH and CK after contusion-induced muscle injuries in mice. In addition, RES and RES + NSAID groups promoted muscle satellite cell regeneration with increase in desmin protein after injury. Our results suggest that resveratrol combined with NSAID potentially improve muscle recovery and may be a potential candidate for further development as an effective clinical treatment for muscle repair.

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