Search

Gallic acid (GA) is a bioactive phytoconstituent that has been reported to prevent a number of diseases. However, there is no systematic review to-date on its anti-diabetic and cardioprotective potential including molecular mechanisms for such activities. This review aims to summarize the anti-diabetic and cardioprotective effects of GA and further propose a molecular mechanism of its anti-diabetic effects. Accumulation of associated literature was conducted through the use of databases including Google Scholar, PubMed, Web of Science, Science Direct and Scopus databases. Articles published until December 2018 were extracted and all the retracted articles were sorted based on the inclusion and exclusion criteria and relevant articles were further consulted for necessary information. We have found substantial investigations in animals and cultured cells that supports anti-diabetic and cardioprotective effects of GA with several underlying mechanisms including antioxidant enzyme systems and non-enzymatic defense mechanisms. The reported antioxidant activity of GA as well as the modulation of some key proteins linked to diabetes could be a part of the mechanisms by which GA showed anti-diabetic effect. In summary, it is evident that GA is one of the promising dietary phytochemicals that could be beneficial for the treatment and management of diabetes and associated myocardial damage. Abbreviation: AGEs: advanced glycation end products; Akt: protein kinase B; ALT: alanine transaminase; AMPKα: AMP-activated protein kinase-alpha; AMPKγ: AMP-activated protein kinase-gamma; ANP: atrial natriuretic peptide; AST: aspartate transaminase; b.w: body weight; CAT: catalase; CK: creatine kinase; CK-MB: creatine kinase-myoglobin binding; CPK: creatine phosphokinase; CRP: C-reactive protein; CsA: cyclosporine A; CVDs: cardiovascular diseases; Cx43: gap junction protein Connexin 43; CYP: cyclophosphamide; CTGF: connective tissue growth factor; DM: diabetes mellitus; D-MI: diabetes with myocardial infraction; DOX: doxorubicin; ECM: extracellular matrix; ERKs: extracellular signal-regulated kinases; GA: gallic acid; GSIS: glucose-stimulated insulin secretion; GLUT4: glucose transporter protein 4; GLUT2: glucose transporter protein 2; GR: glutathione reductase; GSH: reduced Glutathione reductase; GST: glutathione-S-transferase; GATA4: transcription factor GATA-4; HDL: high-density lipoprotein; H9c2(2-1): embryonic rat cardiomyocyte cell line; iNOS: inducible nitric oxide synthase; ISO: isoproterenol; JNKs: c-Jun N-terminal kinases; L-NAME: N-nitro-L-arginine methyl ester; LDL-C: LDL-cholesterol; LDH: lactate dehydrogenase; LDL: low-density lipoprotein; LOOH: lipid hydroperoxides; LPO: lipid peroxidation; LV: left ventricular; MDA: malondialdehyde; MHC-β: myosin heavy chain beta; MI: myocardial infraction; MMP: matrix metalloproteinase; Na⁺/K⁺-ATPase: sodium-potassium adenosine triphosphatase; Nox2: NADPH oxidase 2; PCO: protein carbonyls; PGC1α: peroxisome proliferator-activated receptor gamma coactivator 1-alpha; PI: plasma insulin; PI3K: phosphatidylinositol 3-kinase; PPARγ: peroxisome proliferator-activated receptors- gamma; RAGE: receptor for AGE; ROS: reactive oxygen species; SC: serum creatinine; SOD: superoxide dismutase; GPx: glutathione peroxidase; SHRs: spontaneously hypertensive rats; STZ: Steptozotocin; TBARS: thiobarbituric acid reactive substances; TC: total cholesterol; TG: triglyceride; TGF-β: transforming growth factor beta; TIMP: tissue inhibitor of metalloproteinases; TNF-α: tumor necrosis factor-alpha; TnI: troponin-I; TZDs: thiazolidinediones; UA: uric acid; UCP2: uncoupling protein 2; XO: xanthine oxidase. [ABSTRACT FROM AUTHOR]

In this study, we investigated the effect of Biochanin A (BioA), an O‐methylated isoflavone on the brown‐fat phenotype formation and on the associated thermogenic program including mitochondrial biogenesis and lipolysis in C3H10T1/2 MSCs. Our data demonstrates that Treatment with BioA in an adipogenic differentiation cocktail induced formation of brown‐fat–like adipocytes from C3H10T1/2 MSCs without treatment with a known browning inducer (rosiglitazone or T3) at an early stage of differentiation. The formation of brown‐fat–like adipocytes by BioA treatment was evidenced by upregulation of key thermogenic markers: Ucp1, Pgc1α, Prdm16, and Pparγ. BioA also increased the expression of beige (Cd137 and Fgf21) and brown (Elovl3 and Zic1)‐specific markers. Additionally, BioA treatment promoted mitochondrial biogenesis, judging by the upregulation of genes; Cox8b, Cidea, Dio2, Sirt1, Opa1, and Fis1. BioA treatment increased the amount of mitochondrial DNA and its encoded proteins: oxidative phosphorylation complexes (I–V); this change was associated with high oxygen consumption by C3H10T1/2 MSCs. A small‐interfering‐RNA–induced gene knockdown and experiments with dorsomorphin‐driven competitive inhibition revealed that BioA exerts the thermogenic action via activation of AMPK signaling. Our study shows the mechanism of BioA‐induced promotion of a brown‐fat phenotype. Nonetheless, clinical research is necessary to validate BioA as a brown‐fat‐like signature inducer. [ABSTRACT FROM AUTHOR]

Traditionally, sesame oil (SO) has been used as a popular food and medicine. The review aims to summarize the antioxidant and antiinflammatory effects of SO and its identified compounds as well as further fatty acid profiling and molecular docking study to correlate the interaction of its identified constituents with cyclooxygenase‐2 (COX‐2). For this, a literature study was made using Google Scholar, Pubmed, and SciFinder databases. Literature study demonstrated that SO has potential antioxidant and antiinflammatory effects in various test systems, including humans, animals, and cultured cells through various pathways such as inhibition of COX, nonenzymatic defense mechanism, inhibition of proinflammatory cytokines, NF‐kB or mitogen‐activated protein kinase signaling, and prostaglandin synthesis pathway. Fatty acid analysis of SO using gas chromatography identified known nine fatty acids. In silico study revealed that sesamin, sesaminol, sesamolin, stigmasterol, Δ5‐avenasterol, and Δ7‐avenasterol (−9.6 to −10.7 kcal/mol) were the most efficient ligand for interaction and binding with COX‐2. The known fatty acid also showed binding efficiency with COX‐2 to some extent (−6.0 to −8.4 kcal/mol). In summary, it is evident that SO may be one of promising traditional medicines that we could use in the prevention and management of diseases associated with oxidative stress and inflammation. [ABSTRACT FROM AUTHOR]

The objective of this work was to formulate a Self Emulsifying Drug Delivery System (SEDDS) of simvastatin, a poorly soluble drug and to evaluate by in vivo, in vitro and ex vivo techniques. Oils and surfactants were screened out depending upon their solubilizing capacity. Among all of the solvents, Capryol 90 showed good solubilizing capacity. It dissolved 105 mg/ml of simvastatin. Tween-80 also showed good solubilizing capacity which was 117 mg/ml. The two excipients were used to prepare simvastatin SEDDS. Formulations were initially checked for the color, clarity and sedimentation. The SEDDS formulations were transparent and clear. Formulation F2 containing 7:3 ( m/m) mixture of Capryol 90/Tween-80 produced smallest micro-emulsion with particles size of 0.074 µm and drug release was higher than other formulation (102% within 20 min). Ex vivo study of the SEDDS formulation was evaluated using guinea pig intestinal sac. Drug diffused from F2 formulation was significantly higher than pure drug ( p < 0.001). In vivo study of SEDDS was performed in albino mice using plasma cholesterol level as a pharmacodynamic marker parameter. The test formulation (F2) appeared remarkable reduction in plasma cholesterol level, after oral administration which showed that SEDDS may be an effective technique for the oral administration of simvastatin. [ABSTRACT FROM AUTHOR]

Estimation of joint angles for human joints is important for many applications in Bioengineering. Most of the existing angular joint sensors rely on the assumption of the knowledge of the type of motion and location of the joint. This paper presents a new design for the measurement of finger joint angular motion. The design presented here consists of an exoskeleton, designed to fit the finger motion, in which we can relate the angular displacement of its links to the change in orientation of the phalanx under consideration. Unlike other designs, the exoskeleton does not need any information about the actual anatomy and dimensions of the hand in order to provide with the angular information. The design is to be used in myoelectrical signal identification.