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Protein kinase B and extracellular signal-regulated kinase contribute to the chondroprotective effect of morroniside on osteoarthritis chondrocytes.

Cheng L, Zeng G, Liu Z, Zhang B, Cui X, Zhao H, Zheng X, Song G, Kang J, Xia C - J. Cell. Mol. Med. (2015)

Bottom Line: The results showed that morroniside enhanced the cell viability and the levels of proliferating cell nuclear antigen expression (PCNA), type II collagen and aggrecan in human OA chondrocytes, indicating that morroniside promoted chondrocyte survival and matrix synthesis.The PI3K/AKT inhibitor LY294002 or the MEK/ERK inhibitor U0126 attenuated the effect of morroniside on human OA chondrocytes, indicating that the activation of AKT and ERK contributed to the regulation of morroniside in human OA chondrocytes.As a consequence, morroniside has chondroprotective effect on OA chondrocytes, and may have the therapeutic potential for OA treatment.

View Article: PubMed Central - PubMed

Affiliation: Zhongshan Hospital, University of Xiamen, Xiamen, Fujian, China.

No MeSH data available.


Related in: MedlinePlus

The role of S6, P70S6K and mTOR in the regulatory mechanism of AKT and ERK in morroniside-treated OA chondrocytes. (A) Cells were pre-treated with LY294002 (25 μM) for 2 hrs prior to treatment with morroniside (0.1 μM) for 24 hrs. The level of p-S6 was then detected by western blotting analysis. (B) Cells were pre-treated with U0126 (100 μM) for 2 hrs prior to treatment with morroniside (100 μM) for 24 hrs, and the levels of p-P70S6K and p-S6 were detected by western blotting analysis. The values represent the mean ± SEM of three to five independent experiments, each yielding similar results (*P < 0.05).
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fig03: The role of S6, P70S6K and mTOR in the regulatory mechanism of AKT and ERK in morroniside-treated OA chondrocytes. (A) Cells were pre-treated with LY294002 (25 μM) for 2 hrs prior to treatment with morroniside (0.1 μM) for 24 hrs. The level of p-S6 was then detected by western blotting analysis. (B) Cells were pre-treated with U0126 (100 μM) for 2 hrs prior to treatment with morroniside (100 μM) for 24 hrs, and the levels of p-P70S6K and p-S6 were detected by western blotting analysis. The values represent the mean ± SEM of three to five independent experiments, each yielding similar results (*P < 0.05).

Mentions: To explore the regulatory mechanism of activated AKT and ERK in morroniside-treated human OA chondrocytes, the mTOR/P70S6K/S6 pathway that is the main pathway to regulate protein synthesis, was investigated. The result of Figure3A showed that morroniside only enhanced the level of p-S6, which was blocked dramatically by Ly294002 (Fig.3A, *P < 0.05, versus those treated only with morroniside). Simultaneously, 100 μM morroniside enhanced the levels of p-P70S6K and p-S6, but not p-mTOR. The addition of U0126 attenuated the morroniside-stimulated increase in p-P70S6K (P = 0.0038) and p-S6 level in human OA chondrocytes (Fig.3B, *P < 0.05, versus those treated with only morroniside). However, U0126 caused a significant increase in p-mTOR and p-P70S6K level (Fig.3B, *P < 0.05, versus the untreated group). Therefore, the regulatory mechanism of AKT and ERK may be associated with the phosphorylation of S6, P70S6K, or mTOR in morroniside-treated OA chondrocytes.


Protein kinase B and extracellular signal-regulated kinase contribute to the chondroprotective effect of morroniside on osteoarthritis chondrocytes.

Cheng L, Zeng G, Liu Z, Zhang B, Cui X, Zhao H, Zheng X, Song G, Kang J, Xia C - J. Cell. Mol. Med. (2015)

The role of S6, P70S6K and mTOR in the regulatory mechanism of AKT and ERK in morroniside-treated OA chondrocytes. (A) Cells were pre-treated with LY294002 (25 μM) for 2 hrs prior to treatment with morroniside (0.1 μM) for 24 hrs. The level of p-S6 was then detected by western blotting analysis. (B) Cells were pre-treated with U0126 (100 μM) for 2 hrs prior to treatment with morroniside (100 μM) for 24 hrs, and the levels of p-P70S6K and p-S6 were detected by western blotting analysis. The values represent the mean ± SEM of three to five independent experiments, each yielding similar results (*P < 0.05).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4549038&req=5

fig03: The role of S6, P70S6K and mTOR in the regulatory mechanism of AKT and ERK in morroniside-treated OA chondrocytes. (A) Cells were pre-treated with LY294002 (25 μM) for 2 hrs prior to treatment with morroniside (0.1 μM) for 24 hrs. The level of p-S6 was then detected by western blotting analysis. (B) Cells were pre-treated with U0126 (100 μM) for 2 hrs prior to treatment with morroniside (100 μM) for 24 hrs, and the levels of p-P70S6K and p-S6 were detected by western blotting analysis. The values represent the mean ± SEM of three to five independent experiments, each yielding similar results (*P < 0.05).
Mentions: To explore the regulatory mechanism of activated AKT and ERK in morroniside-treated human OA chondrocytes, the mTOR/P70S6K/S6 pathway that is the main pathway to regulate protein synthesis, was investigated. The result of Figure3A showed that morroniside only enhanced the level of p-S6, which was blocked dramatically by Ly294002 (Fig.3A, *P < 0.05, versus those treated only with morroniside). Simultaneously, 100 μM morroniside enhanced the levels of p-P70S6K and p-S6, but not p-mTOR. The addition of U0126 attenuated the morroniside-stimulated increase in p-P70S6K (P = 0.0038) and p-S6 level in human OA chondrocytes (Fig.3B, *P < 0.05, versus those treated with only morroniside). However, U0126 caused a significant increase in p-mTOR and p-P70S6K level (Fig.3B, *P < 0.05, versus the untreated group). Therefore, the regulatory mechanism of AKT and ERK may be associated with the phosphorylation of S6, P70S6K, or mTOR in morroniside-treated OA chondrocytes.

Bottom Line: The results showed that morroniside enhanced the cell viability and the levels of proliferating cell nuclear antigen expression (PCNA), type II collagen and aggrecan in human OA chondrocytes, indicating that morroniside promoted chondrocyte survival and matrix synthesis.The PI3K/AKT inhibitor LY294002 or the MEK/ERK inhibitor U0126 attenuated the effect of morroniside on human OA chondrocytes, indicating that the activation of AKT and ERK contributed to the regulation of morroniside in human OA chondrocytes.As a consequence, morroniside has chondroprotective effect on OA chondrocytes, and may have the therapeutic potential for OA treatment.

View Article: PubMed Central - PubMed

Affiliation: Zhongshan Hospital, University of Xiamen, Xiamen, Fujian, China.

No MeSH data available.


Related in: MedlinePlus