Related Experiment Video

Updated: Sep 28, 2025

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
07:15

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

559

N,N-Dimethylformamide inhibits high glucose-induced osteoporosis via attenuating MAPK and NF-κB signalling

Ya Dong Liu1, Jian Feng Liu2, Bin Liu2

  • 1Department of Spine Surgery, The First Hospital of Jilin University, Changchun, China.

Bone & Joint Research
|April 4, 2022
PubMed
Abstract

Insights

N,N-dimethylformamide (DMF) inhibits high glucose-induced osteoporosis by targeting key signaling pathways. This study investigated DMF

Area of Science:

  • Biomedical research
  • Cell biology
  • Endocrinology

Background:

  • Diabetes-induced osteoporosis (DM-OS) is a growing concern.
  • The precise role of N,N-dimethylformamide (DMF) in DM-OS progression is not well understood.
  • Investigating novel therapeutic targets for DM-OS is crucial.

Purpose of the Study:

  • To elucidate the effect of DMF on the development of diabetes-induced osteoporosis.
  • To explore the underlying molecular mechanisms by which DMF influences DM-OS.

Main Methods:

  • Established diabetic mouse models, RAW 264.7 cells, and bone marrow macrophages (BMMs).
  • Assessed DMF's impact using micro-CT, histology, cell viability assays, ELISA, ROS analysis, qRT-PCR, and Western blotting.
  • Investigated the involvement of mitogen-activated protein kinase (MAPK) and nuclear factor kappa B (NF-κB) signaling pathways.

Main Results:

  • DMF treatment inhibited ovariectomy-induced osteoporosis in diabetic mice.
  • DMF reversed high glucose-induced increases in osteoclast differentiation markers and reactive oxygen species (ROS).
  • DMF upregulated antioxidant enzyme expression and attenuated osteoclast differentiation by targeting MAPK and NF-κB signaling.

Conclusions:

  • N,N-dimethylformamide (DMF) demonstrates a protective effect against high glucose-induced osteoporosis.
  • DMF exerts its therapeutic action by modulating MAPK and NF-κB signaling pathways.
  • These findings suggest DMF as a potential therapeutic agent for managing diabetes-induced osteoporosis.
Keywords:
DMFDiabetesDiabetes mellitusOsteoporosisTartrate-resistant acid phosphataseWestern blotbone marrowmacrophagesmicro-CTnuclear factor kappa Bosteoclastsovariectomy

More Related Videos

Effect of Anti-c-fms Antibody on Osteoclast Formation and Proliferation of Osteoclast Precursor In Vitro07:51

Effect of Anti-c-fms Antibody on Osteoclast Formation and Proliferation of Osteoclast Precursor In Vitro

Published on: March 18, 2019

6.1K
Synthesis and Characterization of an Aspirin-fumarate Prodrug that Inhibits NFκB Activity and Breast Cancer Stem Cells13:38

Synthesis and Characterization of an Aspirin-fumarate Prodrug that Inhibits NFκB Activity and Breast Cancer Stem Cells

Published on: January 18, 2017

12.4K

Related Concept Videos

MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
6.3K
NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...
7.9K
Osteoclasts in Bone Remodeling01:31

Osteoclasts in Bone Remodeling

Osteoclasts are cells responsible for bone resorption and remodeling. They originate from hematopoietic progenitor cells present in the bone marrow. Numerous progenitor cells fuse to form multinucleated cells, each with 10-20 nuclei. A single osteoclast has a diameter of 150 to 200 µM. These cells have ruffled borders that break down the underlying bone tissue and release minerals such as calcium into the blood in bone resorption. Osteoclasts cling to bones with their ruffled edges during...
3.3K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
4.1K
cAMP-dependent Protein Kinase Pathways01:25

cAMP-dependent Protein Kinase Pathways

Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
6.7K
Oral Hypoglycemic Agents: Biguanides and Glitazones01:26

Oral Hypoglycemic Agents: Biguanides and Glitazones

Biguanides, particularly metformin (Glucophage), are insulin sensitizers that enhance glucose uptake, thereby reducing insulin resistance. Unlike sulfonylureas, metformin doesn't prompt insulin secretion, which helps to curb hypoglycemia risk. Metformin is beneficial in treating conditions like polycystic ovary syndrome due to its insulin-resistance reduction capability. The drug's primary action involves curtailing hepatic gluconeogenesis, a significant contributor to high blood...
321