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1.
J Appl Microbiol ; 134(1)2023 Jan 23.
Artigo em Inglês | MEDLINE | ID: mdl-36626773

RESUMO

AIMS: Myocardial infarction (MI) is among the main public health problems in the world. This atherosclerotic cardiovascular disease (ASCVD), which seriously endangers human health, progresses to cause heart failure and myocardial fibrosis with a poor prognosis. The gut microbiota plays an important role in health and disease, including obesity and ASCVD. In this study, the protective effect of Lacticaseibacillus rhamnosus GG, known for its anti-inflammatory and antioxidant effects, on isoprenaline (ISO)-induced MI in rats was investigated. METHODS AND RESULTS: Rats were divided into four groups of seven rats in each group as control, ISO, L. rhamnosus, and ISO + L. rhamnosus.The ISO application was made by subcutaneous injection to the rats on the last two days (days 27th and 28th) of the 28-day substance administration. The rats were anesthetized 24 hours after the application of ISO, and blood samples were collected after electrocardiogram (ECG) recordings. To determine myocardial damage and protective effects of L. rhamnosus, serum creatine kinase-MB, cardiac troponin-I, tumor necrosis factor-alpha, interleukin-10, and C-reactive protein (CRP) levels were examined. In addition, ECG recordings were evaluated. While L. rhamnosus had a decreasing effect on cardiac troponin-I, creatine kinase-MB, CRP, and tumor necrosis factor-alpha levels, which increased due to ISO, it had an increasing effect on interleukin-10 levels. Similarly, it decreased the ST-segment elevation caused by ISO while increasing the reduced R wave amplitude.


Assuntos
Lacticaseibacillus rhamnosus , Infarto do Miocárdio , Humanos , Ratos , Animais , Isoproterenol/efeitos adversos , Interleucina-10 , Lacticaseibacillus , Troponina I/efeitos adversos , Fator de Necrose Tumoral alfa/metabolismo , Ratos Wistar , Infarto do Miocárdio/induzido quimicamente , Infarto do Miocárdio/tratamento farmacológico , Infarto do Miocárdio/prevenção & controle , Creatina Quinase/efeitos adversos
2.
J Appl Toxicol ; 41(3): 493-505, 2021 03.
Artigo em Inglês | MEDLINE | ID: mdl-33034066

RESUMO

"Pod-based" e-cigarettes such as JUUL are currently the most prevalent electronic nicotine delivery systems (ENDS) in the United States. JUUL-type ENDS utilize nicotine salts protonated with benzoic acid rather than freebase nicotine. However, limited information is available on the cellular effects of these products. Cytoplasmic Ca2+ is a universal second messenger that controls many cellular functions including cell growth and cell death. Of note, dysregulation of cell Ca2+ homeostasis has been linked with several disease processes including autoimmune disease and several types of cancer. We exposed HEK293T cells and THP-1 macrophage-like cells to different JUUL e-liquids. We evaluated their effects on cellular viability and Ca2+ signaling by measuring fluorescence from calcein-AM/propidium iodide and Fluo-4, respectively. E-liquid autofluorescence was used to look for e-liquid permeation into cells. To identify the mechanisms behind the Ca2+ responses, different inhibitors of Ca2+ channels and phospholipase C signaling were used. JUUL e-liquids caused significant cytotoxic effects, with "Mint" flavor being the most cytotoxic. The Mint flavored e-liquid also caused a significant elevation in cytoplasmic Ca2+ . Using autofluorescence, the permeation of JUUL e-liquids into live cells was confirmed, indicating that intracellular organelles are directly exposed to e-liquids. Further studies identified the endoplasmic reticulum as being the source of e-liquid-induced changes in cytoplasmic Ca2+ . Nicotine salt-based e-liquids cause cytotoxicity and elevate cytoplasmic Ca2+ , indicating that they can exert biological effects beyond what would be expected with nicotine alone. These effects are flavor-dependent, and we propose that flavored e-liquids be reassessed for potential lung toxicity.


Assuntos
Morte Celular/efeitos dos fármacos , Sobrevivência Celular/efeitos dos fármacos , Células Cultivadas/efeitos dos fármacos , Vapor do Cigarro Eletrônico/toxicidade , Sistemas Eletrônicos de Liberação de Nicotina , Aromatizantes/toxicidade , Nicotina/toxicidade , Humanos , Estados Unidos
3.
Neurosciences (Riyadh) ; 21(2): 131-7, 2016 04.
Artigo em Inglês | MEDLINE | ID: mdl-27094523

RESUMO

OBJECTIVE: To investigate the effects of thymoquinone (TQ) in a penicillin-induced epilepsy model in rats. METHODS: This experimental study included 56 adult male Wistar rats. Experiments were performed in the Research Laboratory of the Department of Physiology, Medical School, Duzce University, Duzce, Turkey, between October 2013 and December 2014. Animals were divided into the following 7 groups: sham, control, only thymoquinone, vehicle (Dimethylsulfoxide), and doses of 10, 50, and 100 mg/kg of TQ. After rats were anesthetized, the left part of the skull was removed. A pair of silver/silver chloride electrodes was placed on the somatomotor area, and electrocorticographic recording was started. After 5 minutes basal activity was recorded, and TQ was applied intraperitoneally. At the thirtieth minute after TQ, epileptiform activity was induced by intracortical penicillin. The first spike latency, spike frequency, and the amplitude of epileptiform activity were analyzed statistically. RESULTS: The different doses of TQ significantly increased the latency time to onset of first spike wave, and decreased the frequency, and amplitude of epileptiform activity in the first 20 minutes compared with the control group. CONCLUSION: Thymoquinone shows potential as an antiepileptic drug resulting from its effects of prolonged latency time, and reduced spike wave frequency and amplitude of epileptiform activity.


Assuntos
Benzoquinonas/farmacologia , Epilepsia/induzido quimicamente , Epilepsia/tratamento farmacológico , Nigella sativa/química , Penicilinas/efeitos adversos , Sementes/química , Animais , Masculino , Ratos , Ratos Wistar
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