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The Genus Blumea
Published in Namrita Lall, Medicinal Plants for Cosmetics, Health and Diseases, 2022
Some of the terpenoids isolated from Blumea (Figure 15.3) have been reported to possess anticancer properties. Ten new sesquiterpenoid esters, namely; Blumeaenes A–J (83–82), along with 13 flavonoids, were isolated from aerial parts of B. balsamifera and the structures were determined by analysis of 1D and 2D NMR spectroscopic data. All sesquiterpenoid esters were tested for their inhibitory activity against LPS-induced NO production in RAW264.7 macrophages. Blumeaene A (83), Blumeaene D (86) and Blumeaene E (87) showed a slight inhibitory effect on the production of NO, with IC50 values of 40.06 μg/mL, 46.35 μg/mL and 57.80 μg/mL, respectively while other sesquiterpenes were found inactive (IC50 > 100 μg/mL). Aminoguanidine (positive control) showed IC50 = 1.55 μg/mL under the same experimental conditions. All the sesquiterpenes showed no significant cytotoxicity toward normal RAW264.7 cells at their effective concentration for the inhibition of NO production accessed by MTT assay (Chen et al., 2010).
Anti-Diabetic Drugs
Published in Awanish Kumar, Ashwini Kumar, Diabetes, 2020
(PTB) and ALT-711 (Alagebrium) are two widely known experimental AGE breakers. Another potential drug molecule, Kremezin, was shown to markedly decrease the serum AGE levels in patients. Treatment with Kremezin also attenuated the expression of RAGEs, monocyte chemoattractant protein-1 (MCP-1) and vascular cell adhesion molecule-1 (VCAM-1) on the endothelial cells. Anti-hypertensives such as angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin II receptor blockers (ARBs) decrease the formation of AGEs. Telmisartan was reported to decrease the expression of RAGEs and MCP-1 in the mesangial cells, while it also decreased the production of superoxide ions and other ROS [87]. Aminoguanidine traps the reactive carbonyl moieties, and thus prevents the formation of AGEs. But even today, there is no scientific evidence that aminoguanidine works for humans. Pyridoxamine, on the other hand, has been described to chelate Amadori products such as fructoselysine. It also blocks the oxidation of intermediates in the Amadori reaction and traps the highly reactive carbonyl and dicarbonyl compounds [88]. For those interested in the medicinal chemistry and drug designing aspect of RAGE inhibition, a wide range of compounds have been described in references 88 and 89.
Acute Alveolar Injury: Experimental Models
Published in Joan Gil, Models of Lung Disease, 2020
Finally, the isolated guinea pig lung perfused with buffer containing bovine serum albumin has been shown to release histamine into the effluent vascular perfusate during oleic acid injury if histamine catabolism is blocked by aminoguanidine (Selig et al., 1986). Blocking by aminoguanidine alone without administering OA did not cause this histamine release. Pretreatment with antagonists of H1-histamine receptors significantly reduced lung weight gain and capillary alveolar loss of protein induced by OA. Degranulation of lung mast cells with compound 48/80 in the absence of OA led to a transitory weight increase which was much smaller than that induced by OA and was not associated with increased loss of protein from capillaries to alveoli. Because histamine is known to cause postcapillary vasoconstriction in the lung (Hakim et al., 1979; Linehan et al., 1982) the authors suggested that the increased postcapillary resistance demonstrated during OA injury (Hofman and Ehrhart, 1983) is mediated by this vasoactive amine released by pulmonary mast cells and that the resulting increase in capillary hydrostatic pressure augments fluid and protein loss across the capillary-alveolar barrier directly injured by OA.
Ezetimibe attenuates experimental diabetes and renal pathologies via targeting the advanced glycation, oxidative stress and AGE-RAGE signalling in rats
Published in Archives of Physiology and Biochemistry, 2023
Rabia Nabi, Sahir Sultan Alvi, Arunim Shah, Chandra P. Chaturvedi, Mohammad Faisal, Abdulrahman A. Alatar, Saheem Ahmad, M. Salman Khan
Although the implication of aminoguanidine, standard inhibitor of in-vitro AGEs formation (Nabi et al.2018), has showed various adverse effects in different experimental settings i.e. cell culture, animal models studies and human clinical trials in diabetic kidney disease (Bolton et al.2004, Nabi et al.2019b), the development of anti-AGE therapeutic approach remains open for the management of DN. Ezetimibe (EZ) is well reckoned for its pleiotropic pharmacological actions i.e. diminishing the circulatory lipid levels via inhibition of intestinal cholesterol absorption, maintaining redox balance, and inflammatory markers in diabetic and ASCVD patients (Sarigianni et al.2010, Giugliano et al.2018). However, a latest report suggested that administration of EZ also decreases the insulin resistance in patients suffering with metabolic syndrome (Nakamura et al.2019). Recently, we demonstrated that EZ exhibits strong in-vitro anti-glycation potential as well as also protects HEK-293 cells against LDL-AGEs-stimulated reactive oxygen species (ROS) generation and AGEs-RAGE-associated signalling (Nabi et al.2018, 2019b). Except our recent in-vitro findings, there is no report that documented the in-vivo effect of EZ on AGEs-induced diabetic microvascular complications. Therefore, in continuation of our above findings, the current in-vivo study was premeditated to uncover the protective role of EZ against the AGEs-related pathologies via targeting distinct biochemical markers and AGEs-RAGE-associated signalling in experimental diabetic rat model.
Antiglycoxidative properties of amantadine – a systematic review and comprehensive in vitro study
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2023
Miłosz Nesterowicz, Małgorzata Żendzian-Piotrowska, Jerzy Robert Ładny, Anna Zalewska, Mateusz Maciejczyk
Well-known glycation inhibitors and antioxidants were used to compare amantadine’s ability to protect against carbonyl stress. Aminoguanidine prevents glycation through competition, dicarbonyl scavenging, as well as antioxidant activity due to the occurrence of a guanidinium group117. ALA or its reduced form, dihydro-lipoic acid, neutralises ROS and regenerates vitamin C and GSH, which, in turn, can utilise vitamin E118. NAC is a precursor of GSH and may act as a direct ROS-scavenger119. AA owes its antioxidant properties to its ability to donate electrons. Strong reducing properties of AA contribute to its reactivity towards ROS120. In this research, we showed that amantadine has significantly lower antioxidant and antiglycation effect than all ROS scavengers (ALA, NAC, AA) and protein glycation inhibitors (aminoguanidine). Although amantadine does not increase the total antioxidant activity (DPPH and TAC), it should be noted that the compound scavenges HO• and H2O2 at the level of about 50–65%. Amantadine can therefore exhibit antioxidant activity, although it is weaker than the commonly used antioxidants. Moreover, our study confirms previous reports on the proglycation properties of AA51. It is postulated that the ascorbyl radical contributes to protein glycation51,121.
3-Arylcoumarin inhibits vascular calcification by inhibiting the generation of AGEs and anti-oxidative stress
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2022
YuFei Li, Yinbo Pan, Liying Wang, Xiaojing Wang, Haiping Chu, Yan Li, Jie Sun, Yanling Mu
Cells were seeded on a 24-well plate at a density of 5.0 × 104 cells/well, and the normal control group (HASMCs normal culture), vehicle control group (HASMCs + 5‰ DMSO), and calcification induction group (HASMCs + 100 mg/L AGEs-BSA), negative control group (HASMCs + 100 mg/L AGEs-BSA +5‰ DMSO), positive control group (HASMCs + 100 mg/L AGEs-BSA +5‰ DMSO + AGH6.25 mg/L), compounds 1–44 In the interference group (HASMCs + 100 mg/L AGEs-BSA + 5‰ DMSO + compound 6.25 mg/L), after the cell culture of each group is completed, it is determined according to the alkaline phosphatase activity determination kit. (Note: Aminoguanidine hydrochloride is an inhibitor of AGEs production. Studies have shown that it can inhibit the glycosylation modification of proteins in the body and has obvious preventive and therapeutic effects on diabetic vascular complications18. After the MTT assay, DMSO at this concentration had no significant effect on cell proliferation rate).