Int. J. Mol. Sci. 2012, 13(6), 7776-7787; doi:10.3390/ijms13067776
Article

Polydatin Attenuates Hypoxic Pulmonary Hypertension and Reverses Remodeling through Protein Kinase C Mechanisms

Qing Miao 1,† email, Xiao-Peng Shi 2,† email, Ming-Xiang Ye 3,† email, Jin Zhang 4 email, Shan Miao 1 email, Si-Wang Wang 1,* email, Bo Li 3 email, Xiu-Xiu Jiang 3 email, Song Zhang 1 email, Nan Hu 5 email, Juan Li 6 email and Jian Zhang 3,* email
1 Institute of Materia Medica, Fourth Military Medical University, Xi’an 710032, China 2 Department of Pharmacy, Xijing Hospital, Fourth Military Medical University, Xi’an 710032, China 3 Department of Pulmonary Medicine, Xijing Hospital, Fourth Military Medical University, Xi’an 710032, China 4 Department of Plastic Surgery, Xijing Hospital, Fourth Military Medical University, Xi’an 710032, China 5 Institute of Stomatology, General Hospital of People’s Liberation Army, Beijing 100853, China 6 Department of Physiology, Fourth Military Medical University, Xi’an 710032, China † These authors contributed equally to this work.
* Authors to whom correspondence should be addressed.
Received: 10 April 2012; in revised form: 11 May 2012 / Accepted: 12 June 2012 / Published: 21 June 2012
(This article belongs to the Section Bioactives and Nutraceuticals)
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Abstract: Hypoxic pulmonary hypertension is a life-threatening emergency if untreated. Consistent pulmonary hypertension also leads to arteries and ventricular remodeling. The clinical therapeutic strategy for pulmonary hypertension and the corresponding remodeling mainly interacts with NO, angiotensin II (Ang II) and elevated endothelin (ET) targets. In the present study, we evaluated the effects of polydatin on hypoxia-induced pulmonary hypertension. It was observed that polydatin attenuated hypoxic pulmonary hypertension, reversed remodeling, and regulated NO, Ang II, ET contents in the serum and lung samples. However, forced activation of PKC signaling by its selective activator thymeleatoxin (THX) could abate the effects of polydatain. These results suggest that polydatin might be a promising candidate for hypoxic pulmonary treatment through interaction with PKC mechanisms.
Keywords: hypoxic pulmonary hypertension; remodeling; polydatin; protein kinase C

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Cite This Article

MDPI and ACS Style

Miao, Q.; Shi, X.-P.; Ye, M.-X.; Zhang, J.; Miao, S.; Wang, S.-W.; Li, B.; Jiang, X.-X.; Zhang, S.; Hu, N.; Li, J.; Zhang, J. Polydatin Attenuates Hypoxic Pulmonary Hypertension and Reverses Remodeling through Protein Kinase C Mechanisms. Int. J. Mol. Sci. 2012, 13, 7776-7787.

AMA Style

Miao Q, Shi X-P, Ye M-X, Zhang J, Miao S, Wang S-W, Li B, Jiang X-X, Zhang S, Hu N, Li J, Zhang J. Polydatin Attenuates Hypoxic Pulmonary Hypertension and Reverses Remodeling through Protein Kinase C Mechanisms. International Journal of Molecular Sciences. 2012; 13(6):7776-7787.

Chicago/Turabian Style

Miao, Qing; Shi, Xiao-Peng; Ye, Ming-Xiang; Zhang, Jin; Miao, Shan; Wang, Si-Wang; Li, Bo; Jiang, Xiu-Xiu; Zhang, Song; Hu, Nan; Li, Juan; Zhang, Jian. 2012. "Polydatin Attenuates Hypoxic Pulmonary Hypertension and Reverses Remodeling through Protein Kinase C Mechanisms." Int. J. Mol. Sci. 13, no. 6: 7776-7787.

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