Metformin in combination with genistein ameliorates skeletal muscle inflammation in high-fat diet fed c57BL/6 mice

Aliabadi, Masoume; Zamani-Garmsiri, Fahimeh; Panahi, Ghodratollah; Tehrani, Sadra Samavarchi; Meshkani, Reza

doi:10.1016/j.cyto.2021.155638

Cited by 10 publications

(7 citation statements)

References 34 publications

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“…In our study, we confirmed that the disordered glucose and lipid metabolism in obese mice were restored by metformin treatment, which is in line with the investigations from the other groups [ 62 , 63 ]. In addition, the bone protective effect conferred by metformin was comparable to that of lycopene, including an improvement in the bone microstructure, biomechanical strength, and material profiles in obesity-induced hyperglycemia mice.…”

Section: Discussionsupporting

confidence: 92%

Lycopene Improves Bone Quality and Regulates AGE/RAGE/NF-кB Signaling Pathway in High-Fat Diet-Induced Obese Mice

Xia

Zhu

Zhang

et al. 2022

Oxidative Medicine and Cellular Longevity

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Objective. This study was aimed at examining the effects of lycopene on bone metabolism in high-fat diet (HFD)- induced obese mice and to identify the potential underlying mechanisms. Methods. Mice were fed a HFD for 12 weeks and then continue with or without lycopene intervention (15 mg/kg) for additional 10 weeks. The effects of lycopene on blood glucose and lipid metabolism, as well as serum levels of total antioxidant capacity (T-AOC), superoxide dismutase (SOD), and malondialdehyde (MDA) were determined by biochemical assays. Bone histomorphological features and osteoclast activity were assessed by hematoxylin/eosin and tartrate-resistant acid phosphatase staining. Bone microstructure at the proximal tibial metaphysis and diaphysis was determined by microcomputed tomography. Tibial biomechanical strength and material profiles were measured by a three-point bending assay and Fourier transform infrared spectroscopy. Protein expressions involved in the AGE/RAGE/NF-кB signaling pathway were determined by western blot and/or immunohistochemical staining. Results. Lycopene consumption reduced body weight gain and improved blood glucose and lipid metabolism in HFD-induced obese mice. In addition, lycopene treatment preserved bone biomechanical strength, material profiles, and microarchitecture in obese mice. Moreover, these alterations were associated with an increase in serum levels of T-AOC and SOD, and a decline in serum levels of MDA, as well as a reduction of AGEs, RAGE, cathepsin K, and p-NF-кBp65 and NF-кBp65 expressions in the femurs and tibias of obese mice. Conclusion. Lycopene may improve bone quality through its antioxidant properties, which may be linked with the regulation of the AGE/RAGE/NF-кB signaling pathway in obese mice. These results suggest that lycopene consumption may be beneficial for the management of obesity-induced osteoporosis.

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Section: Discussionsupporting

confidence: 92%

Lycopene Improves Bone Quality and Regulates AGE/RAGE/NF-кB Signaling Pathway in High-Fat Diet-Induced Obese Mice

Xia

Zhu

Zhang

et al. 2022

Oxidative Medicine and Cellular Longevity

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“…H. Zhang et al found that genistein inhibits ox-LDL-induced inflammation in HUVECc by inhibiting the NF-κB pathway [26]. It is found to inhibit skeletal muscle inflammation in high-fat diet-fed c57BL/6 mice when combined with metformin [27]. Genistein-loaded nanofibers have been reported to protect spinal cord tissue following experimental injury in rats [28].…”

Section: Discussionmentioning

confidence: 99%

Genistein Protects against Spinal Cord Injury in Mice by Inhibiting Neuroinflammation via TLR4-Mediated Microglial Polarization

Yao

et al. 2022

Applied Bionics and Biomechanics

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Objective. The present study was designed to study the effect of genistein on spinal cord injury (SCI) in mice and to explore its underlying mechanisms. Methods. We established SCI mouse model, and genistein was administered for treatment. We used the Basso, Beattie, and Bresnahan (BBB) exercise rating scale to evaluate exercise recovery, and the detection of spinal cord edema was done using the wet/dry weight method. Apoptosis was determined by TUNEL staining, and inflammation was evaluated by measuring inflammatory factors by an ELISA kit. The expression of M1 and M2 macrophage markers was determined using flow cytometry, and the expression of proteins was detected using immunoblotting. Results. Genistein treatment not only improved the BBB score but also reduced spinal cord edema in SCI mice. Genistein treatment reduced apoptosis by increasing Bcl2 protein expression and decreasing Bax and caspase 3 protein expression. It also reduced the expression of inflammatory cytokines (TNF-α, IL-1β, IL-6, and IL-8) in the SCI area of SCI mice. Flow cytometry analysis indicated that genistein treatment significantly decreased the ratio of M1 macrophages (CD45+/Gr-1-/CD11b+/iNOS+) and increased the ratio of M2 macrophages (CD45+/Gr-1-/CD11b+/Arginase 1+) in the SCI area of SCI mice on the 28th day after being treated with genistein. We also found that genistein treatment significantly decreased the expression of TLR4, MyD88, and TRAF6 protein in the SCI area of SCI mice on 28th day after being treated with genistein. Conclusion. Our findings suggested that genistein exerted neuroprotective action by inhibiting neuroinflammation by promoting the activation of M2 macrophages, and its underlying mechanisms might be related to the inhibition of the TLR4-mediated MyD88-dependent signaling pathway.

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“…Because the prevalence of AD is higher in women compared to age-matched men [ 21 ], we chose to use female mice for this study. The neuroprotective effects of genistein on the male brain are of major interest and have been reported [ 38 – 44 ].…”

Section: Discussionmentioning

confidence: 99%

Effects of Genistein and Exercise Training on Brain Damage Induced by a High-Fat High-Sucrose Diet in Female C57BL/6 Mice

Ding

Geetha

et al. 2022

Oxidative Medicine and Cellular Longevity

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In recent decades, a shift in the nutritional landscape to the Western-style diet has led to an unprecedented rise in the prevalence of obesity and neurodegenerative diseases. Consumption of a healthy diet and engaging in regular physical activity represents safe and affordable approaches known to mitigate the adverse consequences of the Western diet. We examined whether genistein treatment, exercise training, and a combination treatment (genistein and exercise training) mitigated the effects of a Western diet-induced by high-fat, high-sugar (HFHS) in brain of female mice. HFHS increased the amyloid-beta (Aβ) load and phosphorylation of tau, apoptosis, and decreased brain-derived neurotrophic factor (BDNF) levels. Exercise training and genistein each afforded modest protection on Aβ accumulation and apoptosis, and both increased BDNF. The greatest neuroprotective effect occurred with combination treatment. BDNF and all markers of Aβ accumulation, phosphorylation of tau, and apoptosis were improved with combined treatment. In a separate series of experiments, PC12 cells were exposed to high glucose (HG) and palmitate (PA) to determine cell viability with genistein as well as in the presence of tamoxifen, an estrogen receptor antagonist, to assess a mechanism of action of genistein on cell apoptosis. Genistein prevented the neurotoxic effects of HG and PA in PC12 cells and tamoxifen blocked the beneficial effects of genistein on apoptosis. Our results indicate the beneficial effects of genistein and exercise training on HFHS-induced brain damage. The benefits of genistein may occur via estrogen receptor-mediated pathways.

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Metformin in combination with genistein ameliorates skeletal muscle inflammation in high-fat diet fed c57BL/6 mice

Cited by 10 publications

References 34 publications

Lycopene Improves Bone Quality and Regulates AGE/RAGE/NF-кB Signaling Pathway in High-Fat Diet-Induced Obese Mice

Lycopene Improves Bone Quality and Regulates AGE/RAGE/NF-кB Signaling Pathway in High-Fat Diet-Induced Obese Mice

Genistein Protects against Spinal Cord Injury in Mice by Inhibiting Neuroinflammation via TLR4-Mediated Microglial Polarization

Effects of Genistein and Exercise Training on Brain Damage Induced by a High-Fat High-Sucrose Diet in Female C57BL/6 Mice

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