Sparcle, SRA, Structure, Taxonomy, ToolKit, ToolKitAll, ToolKitBookgh, UniGene . Focussing on the relationships between metformin and pulmonary of mg tar and mg nicotine and deliver 12 mg CO each, whereas Melnik .. is a crucial mechanism in the AMPK-mediated activity of this drug STRUCTURE ACTIVITY RELATIONSHIPS OF NICOTINE ANALOGS AND. Erythrina ALKALOIDS ON THE ALPHA 4 BETA 2 NICOTINIC ACETYLCHOLINE. Metformin is the drug of choice for obese NIDDM (non-insulin dependent diabetes mellitus) patients. initially in , the s in Europe, and in in the USA. Structure Metformin administration also increases AMPK activity in skeletal muscle. of Metformin can be increased when it is combined with Nicotine.
The slightly electrolytic value may be due to the contribution of the one chloride anion in the outer sphere of chelating skeleton of the Cr III metformin complex. The infrared absorption bands are one of the important tools of analyses used for determining the mode of chelations. The most significant bands of metformin HCl ligand can be classified into two groups: According to the two fundamental vibrational groups mentioned above, the metformin HCl free ligand can be interpreted as follows: Usually the frequency of this vibration decreases in the presence of the hydrogen bond [ 28 ].
The broad bands at and and cm-1 have been assigned to N-H asymmetric and symmetric stretching vibrations, respectively [ 28 ]. The band at cm-1 has been assigned for NH2 in the plane deformation vibrations [ 28 ]. The bands of the medium-to-weak intensities atand cm The medium-to-weak intensity bands in the IR spectra at, and cm Medium-toweak intensity bands at,and cm This indicates that metformin is coordinated to the metal ions through the nitrogen atom of the imino group.
The infrared spectra of distinguish bands of water molecules concerning hydrated Mfn-HCl complex exist with overlapping the characteristic bands of the amino group. Metformin hydrochloride free ligand has absorption in the ultraviolet regions at, and nm and in some cases these bands extends over to higher wavelength region due to conjugation. New bands due to charge transfer spectra from metal to ligand M—L or ligand to metal L—M can be observed and this data can be processed to obtain information regarding the structure and geometry of the complexes .
The transition in visible region located at nm for Cr III complex can be attributed to the ligandto- metal charge transfer bands LMCT from the electronic lone pairs of adjacent nitrogen coordinated to the Cr III ions. The electronic spectrum of the Mfn. This band show a red shift of the absorbance intensity in Cr III complex.
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This clearly indicates the coordination of the imine nitrogen atom with the metal atom. Various ligand field parameters are calculated. Chromium III complex shows magnetic moment in the range 3. This value is close to the spin only value [ 35 ]. Clear large grains are obtained with agglomerates. The distribution of the grain size is homogeneous. The diffractograms collected for these compounds are given in Figure 4.
Synthesis, Characterization and Antidiabetic Activity of Chromium (III) Metformin Complex
The variable diffractograms of CrIII complex can be attributed to the formation of new structure. The particle size was estimated according to the highest value of intensity compared with the other peaks. The mass loss The finalresidual is chromium oxide CrO1.
The kinetic and thermodynamic parameters were determined using non-isothermal methods. The non-isothermal kinetic analysis for the thermal decomposition of Mfn-HCl ligand and Cr III complex in this work was carried out by the application of the Coats-Redfern[ 38 ] and Horowitz-Metzger method [ 39 ] methods.
Initial point temperature of decomposition Ti: Final point temperature of decomposition Tf: This may assist identifying the mechanism of reaction in the decomposition steps taking place in the complex under study. Order of reaction n: From the abnormal values of Z,the reactions of the complexes at the transition-state can be classified as a slow reaction [ 43 ].
The higher stability of the Cr III complex than that of the Mfn-HCl ligand may be due to the formation of two stable 6-membered rings structures in the metal complexes [ 44 ] and the higher is the molecular symmetry the more stable is the molecule [ 45 ]. It was recorded from table 1 that diabetic untreated group elicited highly significant decrease in SOD when compared to normal control group. However, diabetic group treated with Metformin elicited significant decrease in SOD activity when compared with normal control group by However, Chromium salt treated group elicited non-significant decrease in SOD activity when compared with normal control group.
Its protective role depends on the fact that, for a variety of reasons, type 2 diabetes has been associated with certain cancers 5 — 7. In addition, due to the pleiotropic properties of this drug, metformin interferes with various mechanisms involved in the carcinogenesis process see Discussion. The results of epidemiological studies evaluating the cancer protective properties of metformin are rather controversial, and the results of meta-analyses in diabetic patients treated with this drug are not univocal.
For instance, Decensi et al. Likewise, in 11 studies selected by Noto et al.
Metformin - DrugBank
In contrast, Stevens et al. Further on, from the analysis of 37 studies, Zhang et al. In addition, a wealth of experimental studies have shown that metformin is able to inhibit cell growth in cancer cell lines from a variety of tissues as well as in xenografts of human cancers implanted in nude mice 1.
Focussing on the relationships between metformin and pulmonary carcinogenesis, an observational cohort study in metformin users showed a decreased incidence of lung cancer, which however was no longer detectable by adjusting the data for various confounding factors, among which are smoking habits Similarly, a case—control study led to the conclusion that metformin does not alter the risk of lung cancer in diabetic patients Inducing lung tumors in laboratory animals exposed to cigarette smoke CSas a complex mixture, is a difficult task.
We demonstrated that mainstream CS MCS becomes convincingly carcinogenic in Swiss H mice when exposure starts at birth 16which compares favorably to exposure during adulthood We showed that this animal model is suitable to evaluate the efficacy and safety of chemopreventive agents under conditions mimicking 1 an intervention in current smokers, as evaluated by testing the following drugs or natural compounds: Furthermore, using the same mouse strain, we investigated the interplay between exposure to MCS, histopathological alterations, and treatment with cancer chemopreventive agents in defining microRNA miRNA profiles in lung 23 and evaluated the relationship between pulmonary miRNA expression and proteome profiles, systemic cytogenetic damage and lung tumors as related to exposure to MCS and treatment with chemopreventive agents In this study, we applied this murine model in order to explore the molecular and histopathological alterations induced by MCS and their modulation by oral metformin.
Parallel studies were carried out in two laboratories, using the same mouse strain and method of exposure to MCS.
The laboratory in Sofia evaluated modulation by metformin of systemic genotoxic damage, lung tumors, and other histopathological alterations. The results obtained provide evidence that metformin regulates the expression of a number of miRNAs in the lung of smoke-free mice, highlighting its multiple mechanisms of action, and exerts some protective effects toward molecular and histopathological alterations induced by MCS. The drug prevented MCS-induced preneoplastic lesions in both lung and kidney but did not affect the yield of lung tumors.
Newborn mice of this strain are sensitive to the induction of lung tumors by MCS 16 — 1820 — One hundred postweanling mice 50 males and 50 females were used in the Genoa laboratory for the subchronic toxicity study. In the same laboratory, 40 newborn mice 20 males and 20 females were used for evaluating the effect of metformin on intermediate molecular biomarkers in the lung.
A total of newborn mice males and females were used in the Sofia laboratory for evaluating lung tumors and other histopathological lesions, and a subgroup of 60 mice was used for evaluating the systemic genotoxicity. MCS was generated by drawing 15 consecutive puffs, each of 60 mL and lasting 6 sec, by using a syringe connected with the exposure chamber. Each daily session of treatment with MCS involved six consecutive exposures, lasting 10 min each, with 1-min intervals during which a total air change was made.
These doses were selected based on literature data in mouse studies and taking into account the therapeutical doses used in humans. Each metformin dose and the corresponding metformin-free control were administered to 20 postweanling mice 10 males and 10 females. The mice were inspected daily for general appearance and behavior and were weighed at weekly intervals for 6 weeks.
Evaluation of molecular intermediate biomarkers in the lung Four groups of newborn mice, each composed of 10 mice five males and five femaleswere used for evaluating molecular biomarkers, including bulky DNA adducts, oxidative DNA damage, and miRNA expression profiles in the lung, as follows.
MCS-exposed mice receiving metformin after weaning until the end of the experiment. The mice were inspected daily and weighed at weekly intervals.