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Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
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Metformin alleviates hyperglycemia-induced apoptosis and differentiation suppression in osteoblasts through

Lifeng Zheng1, Ximei Shen2, Junjian Ye1

  • 1Department of Orthopedics, the First Affiliated Hospital of Fujian Medical University, Fuzhou 350005, Fujian, China.

Life Sciences
|November 11, 2018
PubMed
Abstract

Insights

Metformin protects osteoblasts from high blood sugar by inhibiting the TLR4/MyD88/NF-κB pathway, improving bone health in diabetic rats. This research clarifies metformin

Area of Science:

  • Endocrinology
  • Cell Biology
  • Bone Biology

Background:

  • Hyperglycemia impairs osteoblast function, leading to bone injury.
  • The precise cellular mechanisms underlying metformin's protective effects are not fully understood.

Purpose of the Study:

  • To investigate metformin's impact on hyperglycemia-induced osteoblast apoptosis and differentiation suppression.
  • To elucidate the role of the Toll-like receptor 4 (TLR4) signaling pathway in metformin's action.

Main Methods:

  • Utilized MC3T3-E1 mouse osteoblast cell line and a diabetic rat model.
  • Manipulated TLR4 expression via siRNA and lentiviral vectors.
  • Employed lipopolysaccharide (LPS) as a TLR4 activator and CLI-095 as a TLR4 inhibitor.

Main Results:

  • Metformin dose-dependently improved osteoblast differentiation and reduced apoptosis in hyperglycemic conditions.
  • Metformin inhibited the expression of TLR4, MyD88, and NF-κB.
  • Modulating TLR4 and NF-κB activity confirmed their involvement in metformin's protective effects on osteoblasts.
  • In diabetic rats, metformin enhanced bone mineral density and reduced TLR4 pathway markers in femur tissues.

Conclusions:

  • Metformin alleviates hyperglycemia-induced osteoblast apoptosis and differentiation suppression.
  • The protective mechanism involves the inhibition of the TLR4/MyD88/NF-κB signaling pathway.
Keywords:
ApoptosisDifferentiationHyperglycemiaMetforminOsteoblastsTLR4

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