Asiaticoside Regulates Toll-Like Receptor 4/Nuclear Factor-Kappa B Signaling Pathway to Relieve Lipopolysccharide-Induced Inflammation and Apoptosis in ATDC5 Cells

2021 ◽  
Vol 19 (4) ◽  
pp. 432-437
Author(s):  
Lin Gao ◽  
Ming Yang ◽  
San Cai ◽  
Liping Gao ◽  
Chunfeng Gui ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Nuclear Factor Kappa B ◽  
Centella Asiatica ◽  
Joint Disease ◽  
Therapeutic Drug ◽  
Nuclear Factor ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Nuclear Factor Kappa ◽  
Bioactive Component

Osteoarthritis is a progressive joint disease characterized by degeneration and destruction of articular cartilage. The incidence of osteoarthritis has increased steadily over the years leading to more than 50% in people over the age of 65. Due to associated side effects of prevailing therapeutics, better drugs are needed for osteoarthritis management. Asiaticoside is a bioactive component isolated from the medicinal plant Centella asiatica. It has been reported to possess neuroprotective, antiulcer, wound healing, anti-inflammatory, antioxidative, and other pharmacological properties. However, the potential of asiaticoside in the management of osteoarthritis remains to be explored. To this end, we examined the effect of asiaticoside on lipopolysaccharides induced inflammatory injury and apoptosis of chondrocytes. The results show that asiaticoside promotes viability and decrease in apoptosis of ATDC5 cells through decreased production of proinflammatory cytokines and the regulation of toll-like receptor 4/nuclear factor-kappa b signaling pathway. In summary, our results provide the evidence that asiaticoside could serve as a promising therapeutic drug for osteoarthritis treatment.

Baicalin Inhibits Kidney Inflammation in Mice with Diabetic Nephropathy by Modulating Toll-like Receptor 4/Nuclear Factor-Kappa B Signaling Pathway

2020 ◽  
Vol 19 (1) ◽  
pp. 115-119
Author(s):  
Benyong Wang ◽  
Ning Zhao ◽  
Pingyue Ma ◽  
Qunhong Xu ◽  
Qi Chen
Keyword(s):  
Diabetic Nephropathy ◽  
Signaling Pathway ◽  
Nuclear Factor Kappa B ◽  
Kidney Tissue ◽  
Control Group ◽  
Nuclear Factor ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Nuclear Factor Kappa ◽  
Factor Α

We have explored the effect of baicalin, an anti-inflammatory agent, on the outcome of diabetic nephropathy. To this end, we used 6 weeks old C57BL/6J male diabetic mice exhibiting nephropathy. The treatment with baicalin exhibited significant improvement in the renal function, histopathological changes, and expression of inflammatory markers. Moreover, the expression of interleukin-6, tumor necrosis factor-α, and interleukin-1β in kidney tissue of the mice in baicalin group were significantly downregulated compared to the control group (P ‹ 0.05). The expression of toll-like receptor 4, myeloid differentiation factor 88, and nuclear factor-kappa B proteins in the kidney of baicalin-treated mice were remarkably downregulated compared to the control group. Taken together, we conclude that baicalin may exert its protective effect on kidney by inhibiting inflammation through toll-like receptor 4/nuclear factor-kappa B signaling pathway in mice with diabetic nephropathy.

scholarly journals Taurine ameliorates thioacetamide induced liver fibrosis in rats via modulation of toll like receptor 4/nuclear factor kappa B signaling pathway

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Nancy S. Younis ◽  
Amal M. H. Ghanim ◽  
Mohammad A. Elmorsy ◽  
Heba A. Metwaly
Keyword(s):  
Liver Fibrosis ◽  
Signaling Pathway ◽  
Nuclear Factor Kappa B ◽  
Docking Studies ◽  
Nuclear Factor ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Protein Levels ◽  
Nuclear Factor Kappa ◽  
Hydrophobic Binding

AbstractLiver fibrosis is a significant health problem that can cause serious illness and death. Unfortunately, a standard treatment for liver fibrosis has not been approved yet due to its complicated pathogenesis. The current study aimed at assessing the anti-fibrotic effect of taurine against thioacetamide induced liver fibrosis in rats through the modulation of toll like receptor 4/nuclear factor kappa B signaling pathway. Both concomitant and late taurine treatment (100 mg/kg, IP, daily) significantly reduced the rise in serum ALT and AST activities and significantly reversed the decrease in serum albumin and total protein. These results were confirmed by histopathological examinations and immunehistochemical inspection of α-SMA, caspase-3 and NF-κB. The antioxidant potential of taurine was verified by a marked increase of GSH content and a reduction of MDA level in liver tissue. The anti-fibrotic effects of taurine were evaluated by investigating the expression of TLR4, NF-κB. The protein levels of IL-6, LPS, MyD88, MD2, CD14, TGF-β1 and TNF-α were determined. Docking studies were carried out to understand how taurine interacts inside TLR4-MD2 complex and it showed good binding with the hydrophobic binding site of MD2. We concluded that the anti-fibrotic effect of taurine was attributable to the modulation of the TLR4/NF-κB signaling.

Juglone Attenuates Sepsis-Induced Acute Lung Injury via Suppression of the TLR4/Nf-κb Pathway

2020 ◽  
Vol 18 (2) ◽  
pp. 201-206
Author(s):  
Qiu Nan ◽  
Xu Xinmei ◽  
He Yingying ◽  
Fan Chengfen
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Nuclear Factor Kappa B ◽  
Cecal Ligation ◽  
Myeloperoxidase Activity ◽  
Nuclear Factor ◽  
Cecal Ligation And Puncture ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Nuclear Factor Kappa

Sepsis, with high mortality, induces deleterious organ dysfunction and acute lung injury. Natural compounds show protective effect against sepsis-induced acute lung injury. Juglone, a natural naphthoquinone, demonstrates pharmacological actions as a pro-apoptotic substrate in tumor treatment and anti-inflammation substrate in organ injury. In this study, the influence of juglone on sepsis-induced acute lung injury was investigated. First, a septic mice model was established via cecal ligation and puncture, and then verified via histopathological analysis of lung tissues, the wet/dry mass ratio and myeloperoxidase activity was determined. Cecal ligation and puncture could induce acute lung injury in septic mice, as demonstrated by alveolar damage and increase of wet/dry mass ratio and myeloperoxidase activity. However, intragastric administration juglone attenuated cecal ligation and puncture-induced acute lung injury. Secondly, cecal ligation and puncture-induced increase of inflammatory cells in bronchoalveolar lavage fluid was also alleviated by the administration of juglone. Similarly, the protective effect of juglone against cecal ligation and puncture-induced acute lung injury was accompanied by a reduction of pro-inflammatory factor secretion in bronchoalveolar lavage fluid and lung tissues. Cecal ligation and puncture could activate toll-like receptor 4/nuclear factor-kappa B signaling pathway, and administration of juglone suppressed toll-like receptor 4/nuclear factor-kappa B activation. In conclusion, juglone attenuated cecal ligation and puncture-induced lung damage and inflammatory response through inactivation of toll-like receptor 4/nuclear factor-kappa B, suggesting a potential therapeutic strategy in the treatment of sepsis-induced acute lung injury.

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