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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

Morroniside activates AKT and ERK in human OA chondrocytes. (A) Cells were treated with different dose of morroniside (0.1, 20 and 100 μM) for 24 hrs. The levels of AKT, ERK, p-AKT and p-ERK were detected by western blotting analysis. (B) Cells were pre-treated with LY294002 (25 μM) for 2 hrs prior to treatment with morroniside (0.1 μM) for 24 hrs. The cell viability was measured by the MTT assay, and the levels of AKT, p-AKT, PCNA, COL2 and AGG were detected by western blotting analysis, respectively. (C) Cells were pre-treated with U0126 (100 μM) for 2 hrs prior to treatment with morroniside (100 μM) for 24 hrs. The cell viability was measured by the MTT assay, and the levels of ERK, p-ERK, PCNA, COL2 and AGG were detected by Western blotting analysis, respectively. The values represent the mean ± SEM of three to five independent experiments, each yielding similar results (*P < 0.05, **P < 0.01).
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fig02: Morroniside activates AKT and ERK in human OA chondrocytes. (A) Cells were treated with different dose of morroniside (0.1, 20 and 100 μM) for 24 hrs. The levels of AKT, ERK, p-AKT and p-ERK were detected by western blotting analysis. (B) Cells were pre-treated with LY294002 (25 μM) for 2 hrs prior to treatment with morroniside (0.1 μM) for 24 hrs. The cell viability was measured by the MTT assay, and the levels of AKT, p-AKT, PCNA, COL2 and AGG were detected by western blotting analysis, respectively. (C) Cells were pre-treated with U0126 (100 μM) for 2 hrs prior to treatment with morroniside (100 μM) for 24 hrs. The cell viability was measured by the MTT assay, and the levels of ERK, p-ERK, PCNA, COL2 and AGG were detected by Western blotting analysis, respectively. The values represent the mean ± SEM of three to five independent experiments, each yielding similar results (*P < 0.05, **P < 0.01).

Mentions: Compared with untreated cells, the levels of total AKT and ERK1/2 expression in morroniside-treated cells were not changed. However, three doses of morroniside (0.1, 20 and 100 μM) significantly up-regulated the level of p-AKT. Only 100 μM morroniside was sufficient to enhance the level of p-ERK1/2 (Fig.2A, *P < 0.05). Furthermore, the addition of LY294002 (25 μM) for 2 hrs dramatically attenuated the morroniside (0.1 μM)-stimulated increase in the cell viability, p-AKT, PCNA, COL2 and AGG level in human OA chondrocytes (Fig.2B, *P < 0.05, **P < 0.01, versus those treated only with morroniside). Similarly, the addition of U0126 (100 μM) for 2 hrs also attenuated the morroniside (100 μM)-stimulated increase in the cell viability, p-ERK, PCNA, COL2 and AGG level in human OA chondrocytes (Fig.2C, *P < 0.05, **P < 0.01, versus those treated only with morroniside). Comparison of the effect of morroniside on p-AKT and p-ERK revealed that they were not synchronized and that p-AKT is more sensitive than p-ERK to morroniside treatment in human OA chondrocytes. Moreover, the inhibitory effect of LY294002 on COL2 expression was stronger than that of U0126 (Fig.2B and C). AKT and ERK activation thus can contribute to the morroniside-stimulated promoting effect on cell viability and matrix synthesis in human OA chcondrocytes.


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)

Morroniside activates AKT and ERK in human OA chondrocytes. (A) Cells were treated with different dose of morroniside (0.1, 20 and 100 μM) for 24 hrs. The levels of AKT, ERK, p-AKT and p-ERK were detected by western blotting analysis. (B) Cells were pre-treated with LY294002 (25 μM) for 2 hrs prior to treatment with morroniside (0.1 μM) for 24 hrs. The cell viability was measured by the MTT assay, and the levels of AKT, p-AKT, PCNA, COL2 and AGG were detected by western blotting analysis, respectively. (C) Cells were pre-treated with U0126 (100 μM) for 2 hrs prior to treatment with morroniside (100 μM) for 24 hrs. The cell viability was measured by the MTT assay, and the levels of ERK, p-ERK, PCNA, COL2 and AGG were detected by Western blotting analysis, respectively. The values represent the mean ± SEM of three to five independent experiments, each yielding similar results (*P < 0.05, **P < 0.01).
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Related In: Results  -  Collection

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fig02: Morroniside activates AKT and ERK in human OA chondrocytes. (A) Cells were treated with different dose of morroniside (0.1, 20 and 100 μM) for 24 hrs. The levels of AKT, ERK, p-AKT and p-ERK were detected by western blotting analysis. (B) Cells were pre-treated with LY294002 (25 μM) for 2 hrs prior to treatment with morroniside (0.1 μM) for 24 hrs. The cell viability was measured by the MTT assay, and the levels of AKT, p-AKT, PCNA, COL2 and AGG were detected by western blotting analysis, respectively. (C) Cells were pre-treated with U0126 (100 μM) for 2 hrs prior to treatment with morroniside (100 μM) for 24 hrs. The cell viability was measured by the MTT assay, and the levels of ERK, p-ERK, PCNA, COL2 and AGG were detected by Western blotting analysis, respectively. The values represent the mean ± SEM of three to five independent experiments, each yielding similar results (*P < 0.05, **P < 0.01).
Mentions: Compared with untreated cells, the levels of total AKT and ERK1/2 expression in morroniside-treated cells were not changed. However, three doses of morroniside (0.1, 20 and 100 μM) significantly up-regulated the level of p-AKT. Only 100 μM morroniside was sufficient to enhance the level of p-ERK1/2 (Fig.2A, *P < 0.05). Furthermore, the addition of LY294002 (25 μM) for 2 hrs dramatically attenuated the morroniside (0.1 μM)-stimulated increase in the cell viability, p-AKT, PCNA, COL2 and AGG level in human OA chondrocytes (Fig.2B, *P < 0.05, **P < 0.01, versus those treated only with morroniside). Similarly, the addition of U0126 (100 μM) for 2 hrs also attenuated the morroniside (100 μM)-stimulated increase in the cell viability, p-ERK, PCNA, COL2 and AGG level in human OA chondrocytes (Fig.2C, *P < 0.05, **P < 0.01, versus those treated only with morroniside). Comparison of the effect of morroniside on p-AKT and p-ERK revealed that they were not synchronized and that p-AKT is more sensitive than p-ERK to morroniside treatment in human OA chondrocytes. Moreover, the inhibitory effect of LY294002 on COL2 expression was stronger than that of U0126 (Fig.2B and C). AKT and ERK activation thus can contribute to the morroniside-stimulated promoting effect on cell viability and matrix synthesis in human OA chcondrocytes.

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