Leonurine Hydrochloride Suppresses Inflammatory Responses and Ameliorates Cartilage Degradation in Osteoarthritis via NF-κB Signaling Pathway

Chen, Cheng; Zhu, Zhenglin; Hu, Ning; Liang, Xi; Huang, Wei

doi:10.1007/s10753-019-01104-z

Cited by 14 publications

(9 citation statements)

References 36 publications

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“…Interestingly, leonurine can reduce bone loss by inhibiting osteoclast differentiation and promoting 3T3-L1 cell differentiation [ 20 , 21 ]. Our previous research confirmed the contribution of leonurine to osteoblast proliferation and differentiation [ 19 ]. However, the possible ability of leonurine in BMSCs to prevent osteoporosis through the antioxidative effect is still unclear.…”

Section: Introductionsupporting

confidence: 87%

“…Leonurine is a natural chemical compound extracted from the traditional Chinese medicine leonuri. Its high effeciency in the antioxidative effect has drawn much attention, including for cardiovascular diseases, antherosclerosis, ischemic stroke [ 17 , 18 , 19 ], etc. Interestingly, leonurine can reduce bone loss by inhibiting osteoclast differentiation and promoting 3T3-L1 cell differentiation [ 20 , 21 ].…”

Section: Introductionmentioning

confidence: 99%

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Leonurine Protects Bone Mesenchymal Stem Cells from Oxidative Stress by Activating Mitophagy through PI3K/Akt/mTOR Pathway

Zhao

Peng

Wang

et al. 2022

Cells

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Osteoporosis bears an imbalance between bone formation and resorption, which is strongly related to oxidative stress. The function of leonurine on bone marrow-derived mesenchymal stem cells (BMSCs) under oxidative stress is still unclear. Therefore, this study was aimed at identifying the protective effect of leonurine on H2O2 stimulated rat BMSCs. We found that leonurine can alleviate cell apoptosis and promote the differentiation ability of rat BMSCs induced by oxidative stress at an appropriate concentration at 10 μM. Meanwhile, the intracellular ROS level and the level of the COX2 and NOX4 mRNA decreased after leonurine treatment in vitro. The ATP level and mitochondrial membrane potential were upregulated after leonurine treatment. The protein level of PINK1 and Parkin showed the same trend. The mitophage in rat BMSCs blocked by 3-MA was partially rescued by leonurine. Bioinformatics analysis and leonurine-protein coupling provides a strong direct combination between leonurine and the PI3K protein at the position of Asp841, Glu880, Val882. In conclusion, leonurine protects the proliferation and differentiation of BMSCs from oxidative stress by activating mitophagy, which depends on the PI3K/Akt/mTOR pathway. The results showed that leonurine may have potential usage in osteoporosis and bone defect repair in osteoporosis patients.

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Section: Introductionsupporting

confidence: 87%

Section: Introductionmentioning

confidence: 99%

Leonurine Protects Bone Mesenchymal Stem Cells from Oxidative Stress by Activating Mitophagy through PI3K/Akt/mTOR Pathway

Zhao

Peng

Wang

et al. 2022

Cells

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“…Therefore, this method does not meet the requirements because the signal pathway target of the present study is the p38 MAPK pathway. There have been many studies using 10 ng ml IL-1β for the induction of normal chondrocytes for 24 h to successfully obtain degenerated chondrocytes (37,38). This method uses inflammatory factors to directly stimulate the cells to undergo inflammatory changes, which is similar to the pathogenesis of OA with high modeling success rate, and it is also one of the most widely used methods in research.…”

Section: Discussionmentioning

confidence: 99%

Quercetin suppresses apoptosis of chondrocytes induced by IL‑1β via inactivation of p38 MAPK signaling pathway

Wang

Xie

et al. 2021

Exp Ther Med

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The objective of the present study was to investigate the effect of quercetin and evaluate its protective effect on articular cartilage in patients with osteoarthritis (OA), by intervening the p38 pathway. The target factors of quercetin protecting articular cartilage in patients with OA were predicted scientifically and analyzed to predict the possible pathways by using network pharmacology. A pathway predicted to be closely associated with osteoarthritis was chosen for experimental verification in in vitro cells. The optimal intervention drug concentrations were selected by the of Cell Cycle Kit-8 assay, osteoarthritis and inflammatory factors relevant to osteoarthritis, interleukin-1β and tumor necrosis factor-α, were tested by of enzyme-linked immunosorbent assay, and the expression of relevant proteins and mRNA of the p38 signaling pathway was tested by reverse transcription-quantitative PCR and western blotting, following quercetin intervention. It was found that quercetin, at the concentration of 100 umol/l, can decrease inflammatory factors relevant to OA, inhibit the expression of p38, matrix metalloprotease 13 and ADAMTS in the pathway, and promote the expression of collagen Ⅱ. Therefore, it is postulated that quercetin can lower the expression of inflammatory factors in cartilage for the prevention and treatment of OA, and the expression level of relevant factors can be changed positively by blocking the p38 MAPK signaling pathway. Thus, quercetin can promote the repair of degenerative chondrocytes and protect articular chondrocytes.

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“…A wealth of studies has verified that leonurine is beneficial to many systemic diseases of the human body, such as protecting cardiovascular, antioxidant stress, and inhibiting inflammation of the nervous system. 10,12 In the research of malignant tumors, Mao et al illustrated that leonurine could up-regulate the expression of phosphorylated p38 and down-regulate phosphorylated Akt expression through inhibiting mitochondrial pathway, thus suppressing the proliferation and promoting the lung cancer cell apoptosis. 13 Sitarek et al analyzed that the extract of Leonurus sibiricus transgenic roots could induce in different grades of human glioma cell apoptosis.…”

Section: Introductionmentioning

confidence: 99%

<p>Leonurine Promotes Cisplatin Sensitivity in Human Cervical Cancer Cells Through Increasing Apoptosis and Inhibiting Drug-Resistant Proteins</p>

Lin

Pan

et al. 2020

DDDT

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Background: Cisplatin-based neoadjuvant chemotherapy and concurrent radiotherapy and chemotherapy are the main treatment for advanced cervical cancer. However, the development of multidrug resistance (MDR) leads to chemotherapy failure, tumor recurrence and poor survival. In this research, we investigated the effect and corresponding mechanism of leonurine on cisplatin sensitivity of cervical cancer cells. Methods: Anti-cervical cancer efficacy of leonurine and leonurine combined with cisplatin was examined in C33A and Ms751 cells. The cell counting kit-8 assay and bromodeoxyuridine assay were applied for measuring cell proliferation. CompuSyn software was used to calculate the combination index and assess the synergistic effect of leonurine and cisplatin on cell proliferation. The cell cycle distribution and cell apoptosis were analyzed by flow cytometry. The expression of cleaved caspase-3, poly ADP-ribose polymerase (PARP), B-cell lymphoma-2 associated X (BAX), B-cell lymphoma-2 (BCL-2), P glycoprotein (P-Gp) protein and multiple drug resistance protein 1 (MRP1) was analyzed by Western blotting. Results: Leonurine had time-and dose-dependent anti-proliferative effects on C33A and MS751 cells. Leonurine and cisplatin combination was more efficacious in inhibiting the growth of cervical cancer cells than either of the two drugs. The combined application has shown that the cervical cancer cells were arrested at G1 phase after treatments. Moreover, flow cytometry analysis indicated that the combined treatment could cause more cell apoptosis than the single drug treatment. Consistently, combined treatment elevated BAX/BCL-2 ratio, and the expression of BAX, PARP and cleaved caspase-3 proteins. Mechanistic investigations uncovered that the tumor-inhibiting effects of the co-treatment were mediated by repressing MDR, including MRP1 and P-Gp protein, thereby enhancing the efficiency of cisplatin. Conclusion: Leonurine and cisplatin have synergistic antitumorigenic effects on cervical cancer. Combination with leonurine may serve as a novel strategy for enhancing cisplatin sensitivity via the inhibition of the expression of MRP1 and P-Gp.

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Leonurine Hydrochloride Suppresses Inflammatory Responses and Ameliorates Cartilage Degradation in Osteoarthritis via NF-κB Signaling Pathway

Cited by 14 publications

References 36 publications

Leonurine Protects Bone Mesenchymal Stem Cells from Oxidative Stress by Activating Mitophagy through PI3K/Akt/mTOR Pathway

Leonurine Protects Bone Mesenchymal Stem Cells from Oxidative Stress by Activating Mitophagy through PI3K/Akt/mTOR Pathway

Quercetin suppresses apoptosis of chondrocytes induced by IL‑1β via inactivation of p38 MAPK signaling pathway

<p>Leonurine Promotes Cisplatin Sensitivity in Human Cervical Cancer Cells Through Increasing Apoptosis and Inhibiting Drug-Resistant Proteins</p>

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