Filtered By:
Specialty: Molecular Biology
Drug: Metformin
This page shows you your search results in order of date.
Order by Relevance | Date
Total 22 results found since Jan 2013.
Metformin reverses oxidative stress ‑induced mitochondrial dysfunction in pre‑osteoblasts via the EGFR/GSK‑3β/calcium pathway
Int J Mol Med. 2023 Apr;51(4):36. doi: 10.3892/ijmm.2023.5239. Epub 2023 Mar 31.ABSTRACTOxidative stress is one of the main causes of osteoblast apoptosis induced by post‑menopausal osteoporosis. The authors previously found that metformin can reverse the loss of bone mass in post‑menopausal osteoporosis. The present study aimed to further clarify the effects and mechanisms of action of metformin in post‑menopausal osteoporosis under conditions of oxidative stress. Combined with an in‑depth investigation using the transcriptome database, the association between oxidative stress and mitochondrial dysfunction in post...
Source: International Journal of Molecular Medicine - March 31, 2023 Category: Molecular Biology Authors: Fangming Cao Keda Yang Shui Qiu Jie Li Wen Jiang Lin Tao Yue Zhu Source Type: research
Metformin protects against ethanol-induced liver triglyceride accumulation by the LKB1/AMPK/ACC pathway
CONCLUSION: Metformin protects against lipid formation in ALD by activating the LKB1/AMPK/ACC axis.PMID:35733070 | DOI:10.1007/s11033-022-07610-y
Source: Molecular Biology Reports - June 22, 2022 Category: Molecular Biology Authors: Fotian Xie Yuanming Zhong Dongmei Wang Kwok Fai So Jia Xiao Yi Lv Source Type: research
Metformin is a Novel Suppressor for Vimentin in Human Gastric Cancer Cell Line
In this study, AGS gastric cancer cells were treated with metformin and vimentin-specific siRNA (vim-siRNA) for 48 h. The impact of metformin and vim-siRNA on vimentin downregulation in AGS cells were analyzed by quantitative PCR and Western blot. Following treatment with metformin and vim-siRNA, cell motility, migration and invasion abilities of AGS cells were also analyzed. The results showed that inhibition of vimentin due to metformin was comparable with the vim-siRNA. Furthermore, wound-healing and invasion assays showed a significant decrease in migration and invasion of AGS cells following metformin and vim-siRNA tr...
Source: Molecular Medicine - February 18, 2022 Category: Molecular Biology Authors: Shiva Valaee Mehdi Shamsara Mohammad Mehdi Yaghoobi Source Type: research
Metformin alleviates the calcification of aortic valve interstitial cells through activating the PI3K/AKT pathway in an AMPK dependent way
CONCLUSIONS: This study, for the first time, demonstrates that metformin can inhibit AVICs in vitro calcification by activating the PI3K/AKT signaling pathway; this suggests that metformin may provide a potential target for the treatment of CAVD. And the PI3K/AKT signaling pathway emerges as an important regulatory axis in the pathological mechanism of CAVD.PMID:34895136 | DOI:10.1186/s10020-021-00416-x
Source: Molecular Medicine - December 13, 2021 Category: Molecular Biology Authors: Qiao En Huang Zeping Wang Yuetang Wang Xu Wang Wei Source Type: research
Dapagliflozin alleviates cardiac fibrosis through suppressing EndMT and fibroblast activation via AMPK α/TGF-β/Smad signalling in type 2 diabetic rats
This study aimed to evaluate the effect of SGLT2 inhibitor dapagliflozin (DAPA) on DCM especially for cardiac fibrosis and explore the underlying mechanism. In vivo, the model of type 2 diabetic rats was built with high-fat feeding and streptozotocin injection. Untreated diabetic rats showed cardiac dysfunction, increased myocardial fibrosis and EndMT, which was attenuated after treatment with DAPA and metformin. In vitro, HUVECs and primary cardiac fibroblasts were treated with DAPA and exposed to high glucose (HG). HG-induced EndMT in HUVECs and collagen secretion of fibroblasts were markedly inhibited by DAPA. Up-regula...
Source: J Cell Mol Med - June 25, 2021 Category: Molecular Biology Authors: Jingjing Tian Mingjun Zhang Mengying Suo Dian Liu Xuyang Wang Ming Liu Jinyu Pan Tao Jin Fengshuang An Source Type: research
