Shao-Yang-Xi-Bi-Fang Inhibits Chondrocyte Injury and Inflammation in a Rat Model of Osteoarthritis

2021 ◽  
Vol 20 (2) ◽  
pp. 239-246
Author(s):  
Pengfei Shen ◽  
Bin Wang ◽  
Chong Zheng ◽  
Zikang Xie
Keyword(s):  
Protein Kinase ◽  
Rat Model ◽  
Cell Apoptosis ◽  
Morphological Changes ◽  
Protein Kinase B ◽  
Mammalian Target Of Rapamycin ◽  
Protective Role ◽  
Cycle Arrest ◽  
Factor Α ◽  
Necrosis Factor

In the present study, we have examined the protective role and mechanism of Shao-Yang-Xi-Bi-Fang on osteoarthritis induced chondrocyte injury. We observed (a) upregulation of the expression of miR-15a-5p that was positively associated with cell apoptosis and (b) downregulation of protein kinase B protein and mRNA expression in osteoarthritic tissues. Further studies showed that 3'-untranslated regions of the protein kinase B mRNA were the direct target of the miR-15a-5p. The downregulation of the miR-15a-5p led to upregulation of the protein kinase B and mammalian target of rapamycin expression. The Shao-Yang-Xi-Bi-Fang improved the morphological changes, inhibited cell apoptosis, tumor necrosis factor-α, and interleukin-1β in knee osteoarthritis rat model by inducing cell cycle arrest at G1 phase. Taken together, the Shao-Yang-Xi-Bi-Fang inhibited chondrocyte injury and inflammation in a rat model of osteoarthritis via targeting the miR-15a-5p/protein kinase B pathway, providing a new possible therapeutic regimen to osteoarthritis.

Protective effect of irbesartan against doxorubicin-induced nephrotoxicity in rats: implication of AMPK, PI3K/Akt, and mTOR signaling pathways

2018 ◽  
Vol 96 (12) ◽  
pp. 1209-1217 ◽  
Author(s):  
Eman A. Mohamed ◽  
Hebatalla I. Ahmed ◽  
Heba S. Zaky
Keyword(s):  
Protein Kinase ◽  
Protective Effect ◽  
Critical Role ◽  
Mammalian Target Of Rapamycin ◽  
Protective Effects ◽  
Phosphatidylinositol 3 Kinase ◽  
Factor Α ◽  
Amp Activated Protein Kinase ◽  
Renal Expression ◽  
Necrosis Factor

Nephrotoxicity is one of the serious undesirable effects related to doxorubicin (DOX). Herein, we have investigated the potential protective effect of irbesartan (IRB) against chronic nephrotoxicity induced by DOX, and the implication of different mechanistic pathways underlying these effects. Rats were treated with either DOX (2.5 mg/kg i.p., 3 times/week) for 2 weeks, and (or) IRB (40 mg/kg, daily) for 3 weeks. IRB prohibited nephrotoxicity induced by DOX, which was evident by the increase in blood urea nitrogen and creatinine levels and histopathological changes. IRB improved DOX-induced alterations in oxidative status by diminishing lipid peroxidation and upregulating the antioxidant enzymes. Also, upon DOX treatment, the renal expression of tumor necrosis factor-α, interleukin-6, and caspase-3 were significantly increased; IRB diminished DOX-induced alterations in these parameters. Moreover, DOX significantly decreased the expression level of AMP-activated protein kinase (AMPK). Meanwhile, DOX induced activation of phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt/PKB) and mammalian target of rapamycin (mTOR) pathways that cross talked with AMPK. On the contrary, IRB successfully counterbalanced all these effects. Collectively, these outcomes suggest that the modulation of AMPK, PI3K, Akt, and mTOR pathways plays a critical role in conferring the protective effects of IRB against DOX nephrotoxicity.

Lupeol Inhibits Proliferation and Promotes Apoptosis of Ovarian Cancer Cells by Inactivating Phosphoinositide-3-Kinase/Protein Kinase B/ Mammalian Target of Rapamycin Pathway

2020 ◽  
Vol 19 (2) ◽  
pp. 206-210
Author(s):  
Feng Chen ◽  
Bei Zhang
Keyword(s):  
Cell Cycle ◽  
Ovarian Cancer ◽  
Protein Kinase ◽  
Cell Viability ◽  
Cancer Cells ◽  
Protein Kinase B ◽  
Mammalian Target Of Rapamycin ◽  
Target Of Rapamycin ◽  
Ovarian Cancer Cells ◽  
Phosphoinositide 3 Kinase

Lupeol exhibits multiple pharmacological activities including, anticancerous, anti-inflammatory, and antioxidant. The aim of this study was to explore the anticancerous activity of lupeol on ovarian cancer cells and examine its mechanism of action. To this end, increasing concentrations of lupeol on cell viability, cell cycle, and apoptosis in Caov-3 cells were evaluated. Lupeol inhibited cell viability, induced G1 phase arrest in cell cycle, increased cell apoptosis, and inhibited the ratio of phospho-Akt/protein kinase B and phospho-mammalian target of rapamycin/mammalian target of rapamycin. In conclusion, these data suggest that lupeol may play a therapeutic role in ovarian cancer.

scholarly journals Anti-Inflammatory Effect of Simonsinol on Lipopolysaccharide Stimulated RAW264.7 Cells through Inactivation of NF-κB Signaling Pathway

Molecules ◽  
2020 ◽  
Vol 25 (16) ◽  
pp. 3573
Author(s):  
Lian-Chun Li ◽  
Zheng-Hong Pan ◽  
De-Sheng Ning ◽  
Yu-Xia Fu
Keyword(s):  
Nitric Oxide ◽  
Signaling Pathway ◽  
Morphological Changes ◽  
Raw264.7 Cells ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Oxide Synthase ◽  
Necrosis Factor

Simonsinol is a natural sesqui-neolignan firstly isolated from the bark of Illicium simonsii. In this study, the anti-inflammatory activity of simonsinol was investigated with a lipopolysaccharide (LPS)-stimulated murine macrophages RAW264.7 cells model. The results demonstrated that simonsinol could antagonize the effect of LPS on morphological changes of RAW264.7 cells, and decrease the production of nitric oxide (NO), tumor necrosis factor α (TNF-α), and interleukin 6 (IL-6) in LPS-stimulated RAW264.7 cells, as determined by Griess assay and enzyme-linked immunosorbent assay (ELISA). Furthermore, simonsinol could downregulate transcription of inducible nitric oxide synthase (iNOS), TNF-α, and IL-6 as measured by reverse transcription polymerase chain reaction (RT-PCR), and inhibit phosphorylation of the alpha inhibitor of NF-κB (IκBα) as assayed by Western blot. In conclusion, these data demonstrate that simonsinol could inhibit inflammation response in LPS-stimulated RAW264.7 cells through the inactivation of the nuclear transcription factor kappa-B (NF-κB) signaling pathway.

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