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Therapeutic Methods and Therapies TCIM
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1.
Am J Transl Res ; 16(1): 234-254, 2024.
Article in English | MEDLINE | ID: mdl-38322552

ABSTRACT

Type 2 diabetes mellitus (T2DM), a common and frequently occurring disease in contemporary society, has become a global health threat. However, current mainstream methods of prevention and treatment, mainly including oral hypoglycemic drugs and insulin injections, do not fundamentally block the progression of T2DM. Therefore, it is imperative to find new ways to prevent and treat diabetes. Traditional Chinese medicine is characterized by multiple components, pathways, and targets with mild and long-lasting effects. Pharmacological studies have shown that nourishing yin traditional Chinese medicine (NYTCM) can play a positive role in the treatment of T2DM by regulating pathways such as the phosphatidylinositol 3-kinase/serine-threonine kinase, mitogen-activated protein kinase, nuclear factor-kappa B, and other pathways to stimulate insulin secretion, protect and repair pancreatic ß cells, alleviate insulin resistance, ameliorate disordered glucose and lipid metabolism, mitigate oxidative stress, inhibit inflammatory responses, and regulate the intestinal flora. The pharmacologic activity, mechanisms, safety, and toxicity of NYTCM in the treatment of T2DM are also reviewed in this manuscript.

2.
PLoS One ; 8(2): e56407, 2013.
Article in English | MEDLINE | ID: mdl-23437127

ABSTRACT

BACKGROUND: Nuclear factor-κB (NF-κB) is a central transcriptional factor and a pleiotropic regulator of many genes involved in acute lung injury. Andrographolide is found in the plant of Andrographis paniculata and widely used in Traditional Chinese Medicine, exhibiting potently anti-inflammatory property by inhibiting NF-κB activity. The purpose of our investigation was designed to reveal the effect of andrographolide on various aspects of LPS induced inflammation in vivo and in vitro. METHODS AND RESULTS: In vivo, BALB/C mice were subjected to LPS injection with or without andrographolide treatments to induce ALI model. In vitro, MLE-12 cells were stimulated with LPS in the presence and absence of andrographolide. In vivo, pulmonary inflammation, pulmonary edema, ultrastructure changes of type II alveolar epithelial cells, MPO activity, total cells, neutrophils, macrophages, TNF-α, IL-6 and IL-1ß in BALF, along with the expression of VCAM-1 and VEGF were dose-dependently attenuated by andrographolide. Meanwhile, in vitro, the expression of VCAM-1 and VEGF was also reduced by andrographolide. Moreover, our data showed that andrographolide significantly inhibited the ratios of phospho-IKKß/total IKKß, phospho-IκBα/total IκBα and phospho-NF-κB p65/total NF-κB p65, and NF-κB p65 DNA binding activities, both in vivo and in vitro. CONCLUSIONS: These results indicate that andrographolide dose-dependently suppressed the severity of LPS-induced ALI, more likely by virtue of andrographolide-mediated NF-κB inhibition at the level of IKKß activation. These results suggest andrographolide may be considered as an effective and safe drug for the potential treatment of ALI.


Subject(s)
Acute Lung Injury/drug therapy , Acute Lung Injury/metabolism , Diterpenes/therapeutic use , NF-kappa B/metabolism , Protective Agents/therapeutic use , Acute Lung Injury/genetics , Acute Lung Injury/pathology , Alveolar Epithelial Cells/pathology , Alveolar Epithelial Cells/ultrastructure , Animals , Bronchoalveolar Lavage Fluid , Cell Count , Cell Survival/drug effects , Cell Survival/genetics , Cytokines/metabolism , DNA/metabolism , Diterpenes/pharmacology , Down-Regulation/drug effects , Gene Expression Regulation/drug effects , Lipopolysaccharides , Male , Mice , Mice, Inbred BALB C , Peroxidase/metabolism , Pneumonia/complications , Pneumonia/drug therapy , Pneumonia/genetics , Pneumonia/pathology , Protective Agents/pharmacology , Protein Binding/drug effects , Protein Binding/genetics , Pulmonary Edema/complications , Pulmonary Edema/drug therapy , Pulmonary Edema/genetics , Pulmonary Edema/pathology , Transcription Factor RelA/metabolism , Vascular Cell Adhesion Molecule-1/genetics , Vascular Cell Adhesion Molecule-1/metabolism , Vascular Endothelial Growth Factor A/genetics , Vascular Endothelial Growth Factor A/metabolism
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