المؤلفون: L. D. Kuras, H. M. Erstenyuk

المصدر: Біологія тварин, Vol 22, Iss 1, Pp 10-14 (2020)

مصطلحات موضوعية: rats, energy metabolism, cadmium chloride, sodium nitrite, na+, k+-activation, mg2+-dependent atpase, adenosine triphosphate, glucose, lactate dehydrogenase, liver, brain, щури, енергетичний обмін, кадмій хлорид, натрій нітрит, na+-, k+-активуюча, mg2+-залежна атф-аза, аденозинтрифосфорна кислота, глюкоза, лактатдегідрогеназа, печінка, головний мозок, Biology (General), QH301-705.5, Veterinary medicine, SF600-1100

الوصف: The mechanism of action of Cadmium and nitrites is different: Cadmium inhibits the enzyme systems of energy supply by replacing divalent metals; and nitrites enhance the formation of methemoglobin, which disrupts oxygen transport to cells. However, to date, the combined effect of these xenobiotics, in particular on energy metabolism, remains poorly understood. Taking into account the foregoing, the purpose of this study was to find out the state of energy metabolism in the brain and liver of rats under conditions of combined action of cadmium chloride and sodium nitrite. The intoxication was modeled as follows: cadmium chloride was administered intramuscularly. Sodium nitrite was administered with drinking water at a dose of 1/10 of LD50 once a day for 10 days. Animals were divided into two groups: intact and experimental. The material was collected after decapitation under thiopental anesthesia at 1st, 14th, 28th day after the completion of the introduction of toxicants. Indicators of energy metabolism were determined as follows: activity of ATPase, lactate dehydrogenase — enzymatic method; glucose concentration — glucose oxidase method; the level of pyruvic, lactic, adenosine triphosphate (ATP) acids — spectrophotometrically; content of Zn, Cu, Mg — by atomic absorption spectrophotometer. The conducted researches indicate disturbance of energy supply of brain and liver tissues by cadmium-nitrite intoxication, which is confirmed by activation of aerobic oxidation of glucose in the brain, increase of ATP content and activity of ATPase in the investigated organs.

وصف الملف: electronic resource

العلاقة: http://aminbiol.com.ua/index.php/archive/126-archive/bt-22-1-2020/1114-energy-supply-of-laboratoryTest-rats-tissues-at-combined-action-of-cadmium-chloride-and-sodium-nitrite; https://doaj.org/toc/1681-0015Test; https://doaj.org/toc/2313-2191Test

الوصول الحر: https://doaj.org/article/d2726804bfdb43b1b2e8dc31b09750d2Test

المؤلفون: Khalilov, R.¹, Dzhafarova, A.¹, Khizrieva, S.¹

المصدر: Bulletin of Experimental Biology & Medicine. Jul2017, Vol. 163 Issue 3, p334-337. 4p.

مصطلحات موضوعية: *HYPOTHERMIA, *LACTATE dehydrogenase, *CEREBRAL ischemia, *REPERFUSION injury, *CEREBROVASCULAR disease, *ISCHEMIA, *LABORATORY rats, *REPERFUSION

مستخلص: We studied activity and kinetic characteristics of lactate dehydrogenase (LDH) in rat brain under conditions of incomplete global ischemia followed by reperfusion against the background of mild hypothermia. It was found that hypothermia leads to a decrease in LDH activity in the ischemic brain; the maximum velocity of the enzyme-catalyzed activity decreased and Michaelis constant increased, due to which the efficiency of catalysis decreased to the level observed in control rats. Ischemia against the background of hypothermia was accompanied by a decrease in the inhibition constant and narrowing of effective pyruvate concentration range. Blood flow resumption in the ischemic brain against the background of mild hypothermia led to an increase in LDH activity, the maximum reaction velocity increased, and Michaelis constant decreased, which lead to a significant increase in the efficiency of catalysis. This was accompanied by an increase in enzyme inhibition constant and a shift of the optimum on the concentration curve towards lower pyruvate concentrations. [ABSTRACT FROM AUTHOR]

المؤلفون: Tang, Shih-En, Liao, Wen-I, Pao, Hsin-Ping, Hsu, Chin-Wang, Wu, Shu-Yu, Huang, Kun-Lun, Chu, Shi-Jye

المصدر: Frontiers in Pharmacology; 7/15/2021, Vol. 12, p1-15, 15p

مصطلحات موضوعية: REPERFUSION, LUNGS, LUNG injuries, LACTATE dehydrogenase, EPITHELIAL cells, PNEUMONIA, RATS

مستخلص: Background: Poloxamer 188 (P188) possesses anti-inflammatory properties and can help to maintain plasma membrane function. P188 has been reported to exert beneficial effects in the treatment of various disorders. However, the effects of P188 in ischemia/reperfusion (IR)-induced acute lung injury have not been examined. Methods: We investigated the ability of P188 to attenuate IR-induced acute lung injury in rats and hypoxia/reoxygenation (HR) injury in murine epithelial cells. Isolated perfused rat lungs were exposed to 40 min ischemia followed by 60 min reperfusion to induce IR injury. Results: IR led to lung edema, increased pulmonary arterial pressure, promoted lung tissue inflammation and oxidative stress, and upregulated the levels of TNF-α, IL-6 and CINC-1, and increased Lactic dehydrogenase (LDH) activity in bronchoalveolar lavage fluid. IR also downregulated the levels of inhibitor of κB (IκB-α), upregulated nuclear factor (NF)-κB (NF-κB), and promoted apoptosis in lung tissues. P188 significantly suppressed all these effects. In vitro, P188 also exerted a similar effect in murine lung epithelial cells exposed to HR. Furthermore, P188 reduced the number of propidium iodide-positive cells, maintained cell membrane integrity, and enhanced cell membrane repair following HR. Conclusion: We conclude that P188 protects against lung IR injury by suppressing multiple signaling pathways and maintaining cell membrane integrity. [ABSTRACT FROM AUTHOR]

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المؤلفون: Ghazanfari, Alireza, Soodi, Maliheh, Omidi, Ameneh

المصدر: Physiology & Pharmacology; Jul2021, Vol. 25 Issue 2, p154-161, 8p

مصطلحات موضوعية: OXIDATIVE stress, HEPATOTOXICOLOGY, LABORATORY rats, QUERCETIN, INSECTICIDES, LACTATE dehydrogenase, ALKALINE phosphatase

مستخلص: Introduction: Neonicotinoids are a new type of insecticides that have been introduced to the poison market during the last three decades. Acetamiprid (ACT) is a neonicotinoid and widely used for controlling pests. It targets the liver as a toxic agent and damages hepatic tissues through oxidative stress mechanisms. Quercetin is a flavonoid with potent antioxidant and hepatoprotective activity and protects tissues from oxidative damages. Thus, this study is aimed to assess the protective effect of quercetin on acetamiprid-induced hepatotoxicity. Methods: Thirty-six Wistar rats were classified into six groups including control, DMSO, ACT 20, ACT 40, quercetin, and ACT40+quercetin. All treatments were administered orally with gavage for 28 days. Alanine amino transferase (ALT), aspartate amino transferase (AST), alkaline phosphatase (ALP) and lactate dehydrogenase (LDH) enzyme activity was measured in serum as biomarkers of hepatotoxicity. Lipid peroxidation, superoxide dismutase (SOD) enzyme activity and total thiol content were measured in hepatic tissues. Also, hepatic tissue sections were prepared and stained with hematoxylin and eosin and evaluated under optic microscope for any tissue injuries. Results: Findings showed that ACT, especially in high dose (40mg/kg), induced hepatic tissue destruction associated with increased hepatic enzyme activity, except ALP activity, in the serum. Besides, ACT increased the lipid peroxidation and decreased total thiol content and SOD activity, which indicates ACT-induced oxidative stress in hepatic tissues. Also, hepatic tissue injuries were observed in ACT-treated group. All these changes in liver were prevented by quercetin. Conclusion: Because of strong antioxidant properties, quercetin can cope effectively with ACT-induced hepatotoxicity. [ABSTRACT FROM AUTHOR]

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المؤلفون: Zang, Zhen-Zhong, Chen, Li-Mei, Liu, Yuan, Guan, Yong-Mei, Du, Qing, Xu, Pan, Shen, Qian, Yang, Ming, Liu, Hong-Ning, Liao, Zheng-Gen

المصدر: Evidence-based Complementary & Alternative Medicine (eCAM); 6/22/2021, p1-16, 16p, 3 Color Photographs, 4 Diagrams, 2 Charts, 3 Graphs

مصطلحات موضوعية: CYCLOOXYGENASE 2, ENERGY metabolism, MEDICINAL plants, ESSENTIAL oils, MYOCARDIAL ischemia, ANIMAL experimentation, WESTERN immunoblotting, NONSTEROIDAL anti-inflammatory agents, DISTILLATION, PEROXISOME proliferator-activated receptors, SUPEROXIDE dismutase, RATS, GAS chromatography, CELLULAR signal transduction, MASS spectrometry, ENZYME-linked immunosorbent assay, LACTATE dehydrogenase, VASCULAR endothelial growth factors, ADENOSINE monophosphate

مستخلص: Acorus tatarinowii is a traditional aromatic resuscitation drug that can be clinically used to prevent cardiovascular diseases. The volatile oil of Acorus tatarinowii (VOA) possesses important medicinal properties, including protection against acute myocardial ischemia (MI) injury. However, the pharmacodynamic material basis and molecular mechanisms underlying this protective effect remain unclear. Using network pharmacology and animal experiments, we studied the mechanisms and pathways implicated in the activity of VOA against acute MI injury. First, VOA was extracted from three batches of Acorus tatarinowii using steam distillation, and then, its chemical composition was determined by GC-MS. Next, the components-targets and protein-protein interaction networks were constructed using systematic network pharmacology. Gene Ontology (GO) function and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were also conducted in order to predict the possible pharmacodynamic mechanisms. Furthermore, animal experiments including ELISAs, histological examinations, and Western blots were performed in order to validate the pharmacological effects of VOA. In total, 33 chemical components were identified in VOA, and ß-asarone was found to be the most abundant component. Based on network pharmacology analysis, the therapeutic effects of VOA against myocardial ischemia might be mediated by signaling pathways involving COX-2, PPAR-α, VEGF, and cAMP. Overall, the obtained results indicate that VOA alleviates the pathological manifestations of isoproterenol-hydrochloride-induced myocardial ischemia in rats, including the decreased SOD (superoxide dismutase) content and increased LDH (lactic dehydrogenase) content. Moreover, the anti-MI effect of VOA might be attributed to the downregulation of the COX-2 protein that inhibits apoptosis, the upregulation of the PPAR-α protein that regulates energy metabolism, and the activation of VEGF and cAMP signaling pathways. [ABSTRACT FROM AUTHOR]

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المؤلفون: Na, Se Won, Jang, Youn Jae, Hong, Mi Hyeon, Yoon, Jung Joo, Lee, Ho Sub, Kim, Hye Yoom, Kang, Dae Gill

المصدر: Evidence-based Complementary & Alternative Medicine (eCAM); 5/28/2021, p1-10, 10p, 1 Color Photograph, 2 Diagrams, 2 Charts, 3 Graphs

مصطلحات موضوعية: INFLAMMATION prevention, NF-kappa B, HIGH performance liquid chromatography, REPERFUSION injury, CREATININE, T-test (Statistics), STATISTICAL significance, HERBAL medicine, ACUTE kidney failure, TOLL-like receptors, CELLULAR signal transduction, ORAL drug administration, TREATMENT duration, LACTATE dehydrogenase, BLOOD urea nitrogen, DESCRIPTIVE statistics, PLANT extracts, RATS, ANIMAL experimentation, MOLECULAR structure, POLYURIA, DATA analysis software, SIGNAL peptides, DISEASE complications

مستخلص: Joa-gui em (左歸飮, JGE) is known to be effective for treating kidney-yin deficient syndrome. However, there is a lack of objective pharmacological research on improving kidney function. This study was designed to evaluate whether JGE improves renal function and related mechanisms in rats with acute renal injury induced by ischemia/reperfusion (I/R). The acute renal failure (ARF) group was subjected to reperfusion after inserting a clip into the renal artery for 45 min. The ARF + JGE (100 or 200 mg/kg/day) groups were orally administered for four days after their I/R surgery, respectively. JGE treatment suppressed the increase in kidney size in the ARF animal model and alleviated the polyuria symptoms. In addition, to confirm the effect of improving the kidney function of JGE, lactate dehydrogenase levels, blood urea nitrogen/creatinine ratio, and creatinine clearance were measured. As a result, it decreased in the ARF group but significantly improved in the JGE group. Also, as a result of examining the morphological aspects of renal tissue, it was shown that JGE improved renal fibrosis caused by ARF. Meanwhile, it was confirmed that JGE reduced inflammation through the nucleotide-binding oligomerization domain-like receptor pyrin domain containing-3 (NLRP3) and toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-κB) signaling pathways, which are the major causes of acute ischemic kidney injury, thereby improving renal function disorder. The JGE has a protective effect by improving the NLRP3 and TLR4/NF-κB signaling pathway in rats with acute renal dysfunction induced by I/R injury. [ABSTRACT FROM AUTHOR]

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المؤلفون: Yang, Dong, Jiang, Yanzhou, Qian, Haixia, Liu, Xiaomin, Mi, Liguo

المصدر: BioMed Research International; 5/27/2021, p1-8, 8p

مصطلحات موضوعية: TROPONIN, REVERSE transcriptase polymerase chain reaction, LIPOPOLYSACCHARIDES, MYOCARDIUM, ANIMAL experimentation, WESTERN immunoblotting, APOPTOSIS, CREATINE kinase, SEPSIS, RATS, MESSENGER RNA, ENZYME-linked immunosorbent assay, LACTATE dehydrogenase, POLYMERASE chain reaction, DISEASE complications

مستخلص: The aim of this study was to investigate the effect of cardiac troponin I-interacting kinase (TNNI3K) on sepsis-induced myocardial dysfunction (SIMD) and further explore the underlying molecular mechanisms. In this study, a lipopolysaccharide- (LPS-) induced myocardial injury model was used. qRT-PCR was performed to detect the mRNA expression of TNNI3K. Western blot was conducted to quantitatively detect the expression of TNNI3K and apoptosis-related proteins (Bcl-2, Bax, and caspase-3). ELISA was performed to detect the content of lactate dehydrogenase (LDH) and creatine kinase (CK). TUNEL assay was used to detect the apoptosis of H9C2 cells. In LPS-induced H9C2 cells, TNNI3K was up regulated. Besides, the CK activity, the content of LDH, and the apoptosis of H9C2 cells were significantly increased after treatment with LPS. Silencing TNNI3K decreased the LDH release activity and CK activity and inhibited apoptosis of H9C2 cell. Further research illustrated that si-TNNI3K promoted the protein expression of Bcl-2 and decreased the protein expression of Bax and cleaved caspase-3. The study concluded that TNNI3K was upregulated in LPS-induced H9C2 cells. Importantly, functional research findings indicated that silencing TNNI3K alleviated LPS-induced H9C2 cell injury by regulating apoptosis-related proteins. [ABSTRACT FROM AUTHOR]

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المؤلفون: Ashoub, Aliaa H., Abdel-Naby, Doaa H., Safar, Marwa M., El-Ghazaly, Mona A., Kenawy, Sanaa A.

المصدر: Environmental Science & Pollution Research; May2021, Vol. 28 Issue 18, p23287-23300, 14p

مصطلحات موضوعية: INHIBIN, NICOTINE, GAMMA rays, ELLAGIC acid, SEMINIFEROUS tubules, LACTATE dehydrogenase, MALE reproductive organs, RATS

مستخلص: Nicotine is an active pharmacological ingredient in cigarette smoke, which may negatively influence the male reproductive system and fertility. This study aims to investigate the effect of fractionated low-dose radiation (fractionated-LDR) and/or ellagic acid (EA) on nicotine-induced hormonal changes and testicular toxicity in rats. Nicotine was administrated orally (1 mg/kg) for 30 days, afterward, rats were treated with LDR (2 × 0.25 Gy/1-week interval), EA (10 mg/kg, 14 consecutive days p.o.), or a combination of both fractionated-LDR and EA. Rats were sacrificed 24 h after the last dose of treatment, then testes were dissected for histopathology examination, along with some biochemical parameters in serum and testicular tissue were evaluated. Nicotine-induced oxidative stress was evidenced by an increase in testicular thiobarbituric acid reactive substances (TBARS) and a decrease in reduced glutathione (GSH) content. Additionally, the activities of testicular androgenic enzymes were decreased, and the activity of serum lactate dehydrogenase (LDH) was significantly increased. The hormonal changes were verified by a noticeable reduction in follicle-stimulating hormone (FSH), luteinizing hormone (LH), and testosterone serum levels. Histological evaluation revealed that the testicular seminiferous tubules structure was distorted. On the contrary, fractionated-LDR plus EA attenuated the negative changes caused by nicotine observed through biochemical and histological findings. Accordingly, the exposure to fractionated-LDR combined with EA may be a promising candidate for treating hormonal changes and testicular toxicity caused by nicotine. [ABSTRACT FROM AUTHOR]

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المؤلفون: Saka, Waid A., Ayoade, Titilayo E., Akhigbe, Tunmise M., Akhigbe, Roland E.

المصدر: Journal of Basic & Clinical Physiology & Pharmacology; May2021, Vol. 32 Issue 3, p237-246, 10p

مصطلحات موضوعية: CARDIOTOXICITY, TROPONIN, HEART injuries, VEGETABLE oils, ANIMAL experimentation, ORGANIC compounds, INHALATION injuries, SUPEROXIDE dismutase, OXIDATIVE stress, RATS, MALONDIALDEHYDE, WEIGHT gain, PHYTOCHEMICALS, SEEDS, LACTATE dehydrogenase, DESCRIPTIVE statistics, PLANT extracts, CREATININE, GLUTATHIONE peroxidase

مستخلص: Cardiovascular diseases are major causes of non-infectious diseases globally. The use of pesticides has been linked with the high global burden of non-communicable diseases. Despite the indiscriminate exposure to dichlorvos (DDVP) by inhalation, no report exists on its possible cardiotoxic effect. This study investigated the cardiotoxicity of DDVP exposure by inhalation and the possible role of Moringa oleifera seed oil. Twenty-one male rats were randomly assigned into 3 groups. Group A (control) received only standard rat diet and water ad' libitum, group B (DDVP) was exposed to DDVP via inhalation for 15 min daily in addition to rat diet and water, and group C (DDVP + M. oleifera seed oil) received treatment as group B as well as 300 mg/kg of M. oleifera seed oil p.o for 28 days. Significant reductions in body weight gain and cardiac weight were observed in DDVP-exposed animals (p<0.05). Similarly, 28 days of exposure to DDVP led to a significant increase in lactate dehydrogenase, creatinine kinase and troponin (p<0.05). DDVP-exposed rats also showed a significant increase in malondialdehyde, and a significant decline in superoxide dismutase and glutathione peroxidase (p<0.05). However, catalase was comparable in DDVP-exposed and control rats. Histopathological observations of the cardiac tissue revealed that DDVP caused marked fat degeneration and necrosis of the myocardial layer. The changes in DDVP-exposed rats were significantly, though not completely, restored by M. oleifera seed oil administration. This study provides novel mechanistic information on the cardiotoxicity of DDVP inhalation, and the antioxidant potential of M. oleifera seed oil. [ABSTRACT FROM AUTHOR]

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المؤلفون: Liman, Abubakar Alhaji, Salihu, Aliyu, Onyike, Elewechi

المصدر: High Blood Pressure & Cardiovascular Prevention; May2021, Vol. 28 Issue 3, p291-300, 10p

مصطلحات موضوعية: ANTIHYPERTENSIVE agents, HYPERTENSION, BLOOD pressure, BIOMARKERS, C-reactive protein, INTERLEUKINS, METHANOL, ANIMAL experimentation, ARGININE, RATS, OXIDATIVE stress, LACTATE dehydrogenase, PLANT extracts, RAMIPRIL, NITRIC oxide, HEMODYNAMICS, HIGH density lipoproteins, ANGIOTENSIN converting enzyme

مستخلص: Introduction: Most available drugs used for management of hypertension have presented a plethora of challenges which genuinely called for development of therapies from natural sources. Aim: This study investigated the effect of methanol extract of Adansonia digitata fruit (MEADF) pulp on N^G-nitro-l-arginine methyl ester (l-NAME) induced hypertension in rats. Methods: Fourty eight (48) wistar rats divided into six (6) groups (eight rats each) were employed. The induction of hypertension was achieved using l-NAME (40mg//kg body weight) by oral gavages. The induced rats were treated with MEADF pulp (200 and 400 mg/kg body weight) and Ramipril (10 mg/kg) and the remaining three groups serve as control. Serum haemodynamic and biochemical modifiable parameters were determined using standard assay procedures Results: Administration of MEADF to the rats exerted a dose-dependent lowering effect on the elevated systolic blood pressure, diastolic blood pressure, mean arterial pressure and heart rate towards the normal physiological threshold. At 400 mg/kg of MEADF, there was significant (p < 0.05) reduction in serum lipid profile and biomarkers associated with endothelial dysfunction [angiotensin converting enzyme (ACE) activity], inflammation (C-reactive protein and interleukin-1β), oxidative stress (malondialdehyde) and cardiac injury (creatine kinase-MB and lactate dehydrogenase activities). However, serum concentrations of nitric oxide, high density lipoprotein cholesterol, total bilirubin and albumin were not significantly (p < 0.05) different from those found in normal control group. Conclusion: This study therefore demonstrates that MEADF possesses an in vivo ACE inhibitory activity, hypotensive potential and the ability to avert further degeneration of biochemical and physiological upsets associated with l-NAME induced hypertension. [ABSTRACT FROM AUTHOR]

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