RESUMO
The ability of extremely low, time-varying electromagnetic field (EMF) to improve germination efficacy was studied in Foxtail millet (Setaria italica) seeds using response surface methodology. An optimal factorial central composite design was chosen to optimize the EMF with three critical factors, viz. frequency, intensity, and duration. The adequacy of the model and fitness was evaluated by analysis of variance and regression coefficients. This model suggested that the factors, frequency, and intensity had a significant impact on germination. Optimal conditions for germination were observed to be 10 Hz frequency, 30,007 nT intensity, and 30-min duration with an observed germination percentage of 93.0, and a predicted germination percentage of 92.92. Magneto-priming was found to increase the germination efficacy (15.66%), shoot length (27.78%), total seedling length (20.30%), seedling dry mass (26.49%), and water uptake (34.48% at 80 min) showing significant output when compared with the control and positive controls. Remarkable improvements were observed in germination parameters such as vigor index-1 (39.14%), vigor index-2 (46.28%), speed of germination (27.52%), and emergence index (12.50%). Magneto-priming was found to reduce the levels of germination-specific enzymes, viz. α-amylase, protease, and dehydrogenase, while it enhanced the levels of antioxidant enzymes, viz. catalase (114.63%) and superoxide dismutase (19.62%), triggering fast germination and early vigor of seedlings. This study clearly showed that EMF priming significantly improved the germination effect and other characteristics of Foxtail millet seeds. Bioelectromagnetics. © 2020 Bioelectromagnetics Society.
Assuntos
Campos Eletromagnéticos , Germinação/efeitos da radiação , Sementes/crescimento & desenvolvimento , Sementes/efeitos da radiação , Setaria (Planta)/crescimento & desenvolvimento , Setaria (Planta)/efeitos da radiação , Antioxidantes/metabolismo , Sementes/metabolismo , Fatores de TempoRESUMO
Herbal plants with antioxidant activities are widely used in Ayurvedic medicine for cardiac and other problems. Arjunolic acid is one such novel phytomedicine with multifunctional therapeutic applications. It is a triterpenoid saponin, isolated earlier from Terminalia arjuna and later from Combretum nelsonii, Leandra chaeton etc. Arjunolic acid is a potent antioxidant and free radical scavenger. The scientific basis for the use of arjunolic acid as cardiotonic in Ayurvedic medicine is proven by its vibrant functions such as prevention of myocardial necrosis, platelet aggregation and coagulation and lowering of blood pressure, heart rate and cholesterol levels. Its antioxidant property combined with metal chelating property protects organs from metal and drug induced toxicity. It also plays an effective role in exerting protection against both type I and type II diabetes and also ameliorates diabetic renal dysfunctions. Its therapeutic multifunctionality is shown by its wound healing, antimutagenic and antimicrobial activity. The mechanism of cytoprotection conferred by arjunolic acid can be explained by its property to reduce the oxidative stress by enhancing the antioxidant levels. Apart from its pathophysiological functions, it possesses dynamic insecticidal property and it is used as a structural molecular framework in supramolecular chemistry and nanoscience. Esters of ajunolic acid function as gelators of a wide variety of organic liquids. Experimental studies demonstrate the versatile effects of arjunolic acid, but still, further investigations are necessary to identify the functional groups responsible for its multivarious effects and to study the molecular mechanisms as well as the probable side effects/toxicity owing to its long-term use. Though the beneficial role of this triterpenoid has been assessed from various angles, a comprehensive review of its effects on biochemistry and organ pathophysiology is lacking and this forms the rationale of this review.
Assuntos
Extratos Vegetais/uso terapêutico , Triterpenos/uso terapêutico , Animais , Anti-Inflamatórios/química , Anti-Inflamatórios/uso terapêutico , Antineoplásicos/química , Antineoplásicos/uso terapêutico , Cardiotônicos/química , Cardiotônicos/uso terapêutico , Humanos , Hipoglicemiantes/química , Hipoglicemiantes/uso terapêutico , Estrutura Molecular , Extratos Vegetais/química , Triterpenos/químicaRESUMO
The pathogenesis of periodontitis involves anaerobic oral bacteria as well as the host response to infection and several drugs have been developed which can curtail these deleterious effects. Proanthocyanidin, a novel flavanoid extracted from grape seeds, has been shown to provide a significant therapeutic effect on endotoxin (Escherichia coli) induced experimental periodontitis in rats. In this study, protective action of different doses of proanthocyanidins was investigated in blood by assaying the reactive oxygen species such as hydrogen peroxide, superoxide anion, myeloperoxidase and lipid peroxides, lysosomal enzyme activities such as cathepsin B, cathepsin D, beta-glucuronidase and acid phosphatase, nonenzymatic antioxidants such as ascorbic acid, alpha-tocopherol, ceruloplasmin, reduced glutathione and antioxidant enzymes such as catalase, superoxide dismutase, glutathione peroxidase and glutathione-s-transferase. Experimental periodontitis rats showed a reduction in body weight and body weight gain could be noticed when they were administered proanthocyanidins. The levels of reactive oxygen species and lysosomal enzymes were found to increase whereas antioxidant levels were decreased significantly in experimental periodontitis. Proanthocyanidins at an effective dose of 30 mg/kg body weight, sc, for 30 days effected a decrease in serum reactive oxygen species, lipid peroxides, lysosomal enzymes, acute phase proteins and an increase in antioxidant levels. Histopathological evidence of experimental periodontitis showed cellular infiltration of inflammatory cells while proanthocyanidin treated groups demonstrated only scattered inflammatory cells and blood vessels. Thus, the results showed that dietary supplementation of proanthocyanidin enhanced the host resistance as well as the inhibition of the biological and mechanical irritants involved in the onset of gingivitis and the progression of periodontal disease.
Assuntos
Endotoxinas/toxicidade , Periodontite/induzido quimicamente , Periodontite/tratamento farmacológico , Proantocianidinas/uso terapêutico , Proteínas de Fase Aguda/imunologia , Animais , Antioxidantes/metabolismo , Peso Corporal , Endotoxinas/imunologia , Escherichia coli/química , Gengiva/efeitos dos fármacos , Gengiva/imunologia , Gengiva/patologia , Peroxidação de Lipídeos , Lisossomos/enzimologia , Masculino , Periodontite/imunologia , Ratos , Ratos Wistar , Espécies Reativas de Oxigênio/metabolismoRESUMO
Arthritis refers to more than 100 disorders of the musculoskeletal system. The existing pharmacological interventions for arthritis offer only symptomatic relief and they are not definitive and curative. Magnetic healing has been known from antiquity and it is evolved to the present times with the advent of electromagnetism. The original basis for the trial of this form of therapy is the interaction between the biological systems with the natural magnetic fields. Optimization of the physical window comprising the electromagnetic field generator and signal properties (frequency, intensity, duration, waveform) with the biological window, inclusive of the experimental model, age and stimulus has helped in achieving consistent beneficial results. Low frequency pulsed electromagnetic field (PEMF) can provide noninvasive, safe and easy to apply method to treat pain, inflammation and dysfunctions associated with rheumatoid arthritis (RA) and osteoarthritis (OA) and PEMF has a long term record of safety. This review focusses on the therapeutic application of PEMF in the treatment of these forms of arthritis. The analysis of various studies (animal models of arthritis, cell culture systems and clinical trials) reporting the use of PEMF for arthritis cure has conclusively shown that PEMF not only alleviates the pain in the arthritis condition but it also affords chondroprotection, exerts antiinflammatory action and helps in bone remodeling and this could be developed as a viable alternative for arthritis therapy.
Assuntos
Artrite Reumatoide/terapia , Terapias Complementares/métodos , Campos Eletromagnéticos , Magnetoterapia , Osteoartrite/terapia , Animais , Artrite Reumatoide/patologia , Artrite Reumatoide/fisiopatologia , Remodelação Óssea , Osso e Ossos/fisiopatologia , Condrócitos/patologia , Matriz Extracelular/patologia , Humanos , Inflamação/terapia , Osteoartrite/patologia , Osteoartrite/fisiopatologia , Manejo da DorRESUMO
Rheumatoid arthritis (RA) is a chronic inflammatory disorder affecting 1% of the population worldwide. Pulsed electromagnetic field (PEMF) has a number of well-documented physiological effects on cells and tissues including antiinflammatory effect. This study aims to explore the antiinflammatory effect of PEMF and its possible mechanism of action in amelioration of adjuvant induced arthritis (AIA). Arthritis was induced by a single intradermal injection of heat killed Mycobacterium tuberculosis at a concentration of 500 microg in 0.1 ml of paraffin oil into the right hind paw of rats. The arthritic animals showed a biphasic response regarding changes in the paw edema volume. During the chronic phase of the disease, arthritic animals showed an elevated level of lipid peroxides and depletion of antioxidant enzymes with significant radiological and histological changes. Besides, plasma membrane Ca(2+) ATPase (PMCA) activity was inhibited while intracellular Ca(2+) level as well as prostaglandin E(2) levels was noticed to be elevated in blood lymphocytes of arthritic rats. Exposure of arthritic rats to PEMF at 5 Hzx4 microT x 90 min, produced significant antiexudative effect resulting in the restoration of the altered parameters. The antiinflammatory effect could be partially mediated through the stabilizing action of PEMF on membranes as reflected by the restoration of PMCA and intracellular Ca(2+) levels in blood lymphocytes subsequently inhibiting PGE(2) biosynthesis. The results of this study indicated that PEMF could be developed as a potential therapy for RA in human beings.
Assuntos
Artrite Experimental/radioterapia , ATPases Transportadoras de Cálcio/metabolismo , Membrana Celular/metabolismo , Campos Eletromagnéticos , Inflamação/radioterapia , Animais , Artrite Experimental/complicações , Dinoprostona/metabolismo , Inflamação/etiologia , Linfócitos/sangue , Masculino , Mycobacterium tuberculosis , Radiografia , Ratos , Espectrometria de Fluorescência , Tarso Animal/diagnóstico por imagem , Tarso Animal/patologiaRESUMO
Matrix metalloproteinases (MMPs) constitute a family of zinc-dependent proteolytic enzymes, which degrade several components of extracellular matrix, in arthritic synovial cells. In cultured synovial fibroblasts, both nitric oxide (NO) and reactive oxygen species (ROS) are potent inducers of MMPs production. PEP1261, a tetrapeptide derivative used in this study, corresponds to residues of 39-42 human lactoferrin. The parent protein lactoferrin is able to inhibit the production of free radicals in rheumatoid joints and it regulates many aspects of inflammation. This study is aimed to examine the effects of PEP1261 on MMP-2 production in the presence of nitric oxide donor in cultured synovial fibroblasts from collagen-induced arthritic rats. PEP1261 affects a significant reduction in nitrite levels as well as in MMP-2 production in SNAP stimulated synovial fibroblasts and this is validated by gelatin zymography and immunoblot analysis. Furthermore, RTPCR analysis has demonstrated that PEP1261 inhibits MMP-2 mRNA expression in SNAP treated synovial fibroblasts. The results of this study suggest that PEP1261 possesses antiarthritic activity by inhibiting nitrite levels as well as MMP-2 expression better than control peptides viz., KRDS and RGDS.
Assuntos
Artrite/metabolismo , Colágeno/química , Fibroblastos/metabolismo , Lactoferrina/química , Metaloproteinase 2 da Matriz/biossíntese , Óxido Nítrico/metabolismo , Fragmentos de Peptídeos/farmacologia , Membrana Sinovial/metabolismo , Animais , Modelos Animais de Doenças , Concentração Inibidora 50 , Lactoferrina/farmacologia , Peptídeos/química , RNA/metabolismo , Ratos , Ratos WistarRESUMO
In this study, the effect of (Boc-Lys (Boc)-Arg-Asp-Ser (tBu)-OtBu), a tetrapeptide derivative (PEP1261) was examined for antiproliferative potency and apoptotic induction. Synovial fibroblasts were isolated from collagen-induced arthritic (CIA) rats and exposed to peptides viz., PEP1261, and parental peptides (KRDS and RGDS). Viability of the cells decreased in the presence of PEP1261 at a lower concentration (0.1 mM) when compared to RGDS and KRDS (1 mM). The treatment of cells with peptides showed induction of apoptosis, resulting in the cleavage of caspase-3 as well as its substrate poly-(ADP-ribose) polymerase (PARP). Pretreatment of cells with caspase-3 inhibitor prevented inhibition of [(3)H] thymidine incorporation, DNA fragmentation, and cleavage of caspase-3 and PARP as confirmed by western blotting as well as annexin-V/PI-staining using flow cytometry. However, caspase-1 and caspase-2 inhibitors did not prevent the peptides from inducing apoptosis indicating that caspase-3 might have a role in the process of apoptosis induced by peptides. Treatment of synovial fibroblasts with nitric oxide donor, S-nitroso-N-acetyl-DL: -penicillamine (SNAP) (500 microM) showed significant elevation of nitric oxide levels and resulted in absence of apoptosis by preventing the inhibition of [(3)H] thymidine incorporation. This was further evidenced by annexin V/propidium iodide (PI) staining and absence of DNA fragmentation, intra cellular caspase-3 activity and PARP cleavage. In contrast, SNAP followed by PEP1261 and parental peptides-induced apoptosis by lowering the levels of nitric oxide. These results suggested that PEP1261 suppressed the proliferation and induced apoptosis in cultured synovial fibroblasts from CIA rats. This study also confirmed that PEP1261 inhibited nitric oxide level in cultured synovial fibroblasts.
Assuntos
Apoptose/efeitos dos fármacos , Artrite/metabolismo , Caspases/metabolismo , Fibroblastos/efeitos dos fármacos , Lactoferrina/farmacologia , Óxido Nítrico/antagonistas & inibidores , Fragmentos de Peptídeos/farmacologia , Animais , Anexina A5/metabolismo , Artrite/induzido quimicamente , Artrite/patologia , Caspase 3 , Proliferação de Células/efeitos dos fármacos , Células Cultivadas , Colágeno Tipo II , Ativação Enzimática , Fibroblastos/metabolismo , Fibroblastos/patologia , Masculino , Óxido Nítrico/metabolismo , Oligopeptídeos/farmacologia , Poli(ADP-Ribose) Polimerases/metabolismo , Ligação Proteica , Ratos , Ratos Wistar , Líquido Sinovial/citologiaRESUMO
Studies were undertaken to find out the effects of low frequency pulsed electromagnetic field (PEMF) in adjuvant induced arthritis (AIA) in rats, a widely used model for screening potential therapies for rheumatoid arthritis (RA). AIA was induced by an intradermal injection of a suspension of heat killed Mycobacterium tuberculosis (500 mug/0.1 ml) into the right hind paw of male Wistar rats. This resulted in swelling, loss of body weight, increase in paw volume as well as the activity of lysosomal enzymes viz., acid phosphatase, cathepsin D, and beta-glucuronidase and significant radiological and histological changes. PEMF therapy for arthritis involved optimization of three significant factors, viz., frequency, intensity, and duration; and the waveform used is sinusoidal. The use of factorial design in lieu of conventional method resulted in the development of an ideal combination of these factors. PEMF was applied using a Fransleau-Braunbeck coil system. A magnetic field of 5 Hz x 4 muT x 90 min was found to be optimal in lowering the paw edema volume and decreasing the activity of lysosomal enzymes. Soft tissue swelling was shown to be reduced as evidenced by radiology. Histological studies confirmed reduction in inflammatory cells infiltration, hyperplasia, and hypertrophy of cells lining synovial membrane. PEMF was also shown to have a membrane stabilizing action by significantly inhibiting the rate of release of beta-glucuronidase from lysosomal rich and sub-cellular fractions. The results indicated that PEMF could be developed as a potential therapy in the treatment of arthritis in humans.
Assuntos
Artrite Experimental/radioterapia , Campos Eletromagnéticos , Fosfatase Ácida/análise , Fosfatase Ácida/efeitos da radiação , Animais , Anti-Inflamatórios não Esteroides/uso terapêutico , Artrite Experimental/imunologia , Artrite Experimental/patologia , Artrite Reumatoide , Peso Corporal , Catepsina D/análise , Catepsina D/efeitos da radiação , Diclofenaco/uso terapêutico , Edema/imunologia , Edema/patologia , Edema/radioterapia , Pé/patologia , Pé/efeitos da radiação , Glucuronidase/análise , Glucuronidase/efeitos da radiação , Membro Posterior/patologia , Membro Posterior/efeitos da radiação , Hiperplasia , Hipertrofia , Lisossomos/enzimologia , Lisossomos/efeitos da radiação , Masculino , Mycobacterium tuberculosis/imunologia , Ratos , Ratos Wistar , Membrana Sinovial/patologia , Membrana Sinovial/efeitos da radiaçãoRESUMO
This study was designed to investigate the protective effect of curcumin (CUR) against isoprenaline induced myocardial ischaemia in rat myocardium. The effect of single oral dose of curcumin (15 mg kg(-1)), administered 30 min before and/or after the onset of ischaemia, was investigated by assessing oxidative stress related biochemical parameters in rat myocardium. Curcumin pre and post-treatment (PPT) was shown to decrease the levels of xanthine oxidase, superoxide anion, lipid peroxides (LPs) and myeloperoxidase while the levels of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST) activities were significantly increased after curcumin PPT. Histopathological and transmission electron microscopical studies also confirmed the severe myocardial damage occurring as a consequence of isoprenaline induced ischaemia and they also showed the significant improvement effected by curcumin PPT. These findings provided evidence that curcumin was found to protect rat myocardium against ischaemic insult and the protective effect could be attributed to its antioxidant properties as well as its inhibitory effects on xanthine dehydrogenase/xanthine oxidase (XD/XO) conversion and resultant superoxide anion production.
Assuntos
Curcumina/farmacologia , Radicais Livres/metabolismo , Isquemia Miocárdica/metabolismo , Animais , Testes de Coagulação Sanguínea , Modelos Animais de Doenças , Feminino , Hemodinâmica/efeitos dos fármacos , Peróxidos Lipídicos/metabolismo , Estrutura Molecular , Isquemia Miocárdica/patologia , Isquemia Miocárdica/fisiopatologia , Estresse Oxidativo/efeitos dos fármacos , Extratos Vegetais/farmacologia , Agregação Plaquetária/efeitos dos fármacos , Ratos , Ratos Wistar , Superóxidos/metabolismo , Trombina/farmacologiaRESUMO
A tetrapeptide derivative PEP1261 [Boc-Lys-(Boc)-Arg-Asp-Ser-(tBu)-OtBu], corresponding to residues 39-42 of human lactoferrin, was tested for its antiinflammatory action in adjuvant induced arthritis in rats. Administration of heat killed Mycobacterium tuberculosis (500 microg/0.1 ml of paraffin oil) intradermally into the foot pad of right hind paw resulted in an increased paw volume and an increase in the levels of reactive oxygen species and beta-glucuronidase as well as a decrease in the antioxidants levels. PEP1261, at an effective dose of 10 mg/kg body wt., exhibited a significant antiarthritic activity as evidenced by lowering of paw volume and inhibited the free radicals toxicity by increasing the antioxidants levels. This peptide derivative was also shown to have a membrane stabilizing action by significantly decreasing the total and free activity of beta-glucuronidase and inhibiting the rate of release of the enzyme from lysosomal rich fraction. Histopathological studies confirmed the above results by showing a decrease in mononuclear cell infiltration, hypertrophy, hyperplasia and pannus formation after PEP1261 treatment in arthritic rats.