Qing Jiang

Educational Background

  • Ph.D., Biochemistry at Washington State University in 1997
  • Postdoc, Biochemistry at Unversity of California, Berkeley in 2001

Awards & Honors

  • Editorial Board of Journal of Nutritional Biochemistry, 2010 - Present
  • University Faculty Scholar, 2014
  • Purdue Entrepreneurial Leadership Academy Fellow from Purdue University, 2011
  • E.L.R. Stokstad Award from the American Society for Nutrition , 2011
  • Postdoctoral Fellowship Award from American Heart Association, 2001
  • Elected Member from Sigma Xi Scientific Research Society, 1997


Chronic inflammation constitutes one of the major etiologies of degenerative diseases including cancer. My laboratory is interested in studying the molecular mechanism of inflammation-associated diseases, and exploring prevention and therapy of these diseases, using nutrition factors including natural forms of vitamin E as well as combinations of vitamin E forms and other antioxidants.

During inflammation, pro-inflammatory eicosanoids including cyclooxygenase-catalyzed prostaglandin E2 (PGE2) and lipoxygenase-catalyzed leukotriene B4 (LTB4), and pro-inflammatory cytokines like TNF-alpha, play the central roles in regulating inflammatory response and inflammation-mediated damage. Eicosanoids generated through cyclooxygenase and lipoxygenase also promote tumorigenesis.

Vitamin E comprises eight structurally related molecules [alpha-, beta-, gamma-, delta-tocopherol, and alpha-, beta-, gamma-, delta-tocotrienol]. Among them, only alpha-tocopherol, the major form of vitamin E in tissues and most supplements, has been extensively studied, but other forms were mostly ignored. We have recently discovered that some non-alpha forms of vitamin E have unique properties which are important to improving human health. For instance, gamma-tocopherol, the major form of vitamin E in US diets, and its major metabolite, but not alpha-tocopherol, exhibit anti-inflammatory effects by inhibiting PGE2 and LTB4 and reducing TNF-alpha in cell culture and a rat inflammation model. We are currently focusing on the following three projects:

1. Vitamin E forms as anti-inflammatory agents
We are currently investigating the interaction between vitamin E molecules and different isoforms of cyclooxygenase and lipoxygenase, as well as the role of vitamin E in gene regulation during inflammation. We are testing the pharmaceutical utilities of vitamin E forms as novel anti-inflammatory agents in animal models.

2. Vitamin E forms as anti-cancer agents
We have recently showed that gamma-tocopherol, but not alpha-tocopherol, inhibits growth and induces cell dealth in prostate and lung cancer cells but has no effect on normal prostate epithelial cells. Our study demonstrates that gamma-tocopherol induce cell death by interrupting sphingolipid synthesis. We are planning to investigate the molecular interaction between vitamin E forms and various key enzymes in the pathway of de novo synthesis of sphingolipids, the role of these enzymes in cell fate, and testing the anti-cancer potential of vitamin E forms in various cancer models in animals.

3. Vitamin E forms and asthma
In airway inflammation in asthma, myeloperoxidase from neutrophils and eosinophil peroxidase from eosinophils generate highly potent oxidants that cause oxidative damage. We are investigating the potential detoxification of the damage caused by these peroxidases by vitamin E forms and other antioxidants. In cells mediating inflammatory response in asthma, the effect and mechanism of antioxidants on key regulatory pathways of inflammation will be studied.

Discovery Publications

  • Wang, Y., Park, N.Y., Jang, Y., Averail, M., and Jiang, Q. (2015) Vitamin E gamma-tocotrienol inhibits cytokine-stimulated NF-kB activation by induction of anti-implammary A20 via stress adaptive response due to modulatio of sphingolipids. J. Immunology. In press.
  • Jiang, Q., (2014) Natural forms of vitamin E: metabolism, antioxidant and anti-inflammatory activities and their role in disease prevention and therapy. Free Rad Biol Med. 72:76-90.
  • Jiang, Q., Jiang, Z., Jones, Y., Jang, Y., Snyder, P., Bain, C., Huang, J., Jannasch, A., Cooper, B., Wang, Y., and Moreland, M. (2013) Gamma-tocopherol attenuates moderate but not severe colitis and suppresses moderate colitis-promoted colon tumorigenesis in mice. Free Rad Biol Med. 65:1069-1077. doi: 10.1016/j.freeradbiomed.2013.08.187. [Epub ahead of print].
  • Wang, Y., and Jiang, Q. (2013) Gamma-tocotrienol inhibits lipopolysaccharide-induced interlukin-6 and granulocyte-colony stimulating factor by suppressing C/EBP-β and NF-κB in macrophages. J Nutr Biochem. 24:1146-52. Other Information.
  • Wang, Y., Moreland, M., Wagner, J.G., Ames, B.N., Illek, B., Peden, D.B. and Jiang, Q. (2012) Vitamin E forms inhibit IL-13/STAT6-induced eotaxin-3 secretion by upregulation of PAR4, an endogenous inhibitor of atypical PKC in human lung epithelial cells. J Nutr Biochem. 23(6):602-8.
  • Gopalan, A., Yu, W., Jiang, Q., Jang, Y., Sanders, B.G., and Kline, K. (2012) Involvement of de novo ceramide synthesis in gamma-tocopherol and gamma-tocotrienol induced apoptosis in human breast cancer cells. Mol Food Nutr Res. 56(12):1803-11. Other Information.
  • Jiang, Q., Rao, X., Kim, C.Y., Freiser, H., Zhang, Q., Jiang, Z., and Li, G. (2011) Gamma-tocotrienol induces apoptosis and autophagy in prostate cancer cells by increasing intracellular dihydrosphingosine and dihydroceramide. Int J Cancer. 130(3):685-93.
  • Jiang, Z., Yin, Y.X., and Jiang, Q. (2011) Natural forms of vitamin E and 13-carboxychromanol, a long-chain vitamin E metabolite, inhibit leukotriene generation from stimulated neutrophils by blocking calcium influx and suppressing 5-lipoxygenase activity, respectively. J Immunology. 186(1173)
  • Freiser, H., and Jiang, Q. (2009) Gamma-tocotrienol and gamma-tocopherol are primarily metabolized to conjugaed 2-(gamma-carboxyethyl)-6-hydroxy-2,7,8-trimethylchroman and sulfated long-chain carboxychromanols in rats. J Nutr. 139:884-9.
  • Freiser, H. and Jiang, Q. (2009) Optimization of the enzymatic hydrolysis and analysis of plasma conjugated gamma-CEHC and sulfated long-chain carboxychromanols, metabolites of vitamin E. Anal Biochem. 388(2):260-5.
  • Jiang, Q., Moreland, M., Ames, B.N., and Yin, X. (2009) A combination of aspirin and gamma-tocopherol is better than that of aspirin and alpha-tocopherol in anti-inflammatory action and attenuating aspirin-caused adverse effects. J Nutr Biochem. 20(11):894-900.
  • Jiang, Q., Yin, X., Lill, M.A., Danielson, M.L., Freiser, H., and Huang, J. (2008) Long-chain carboxychromanols, metabolites of vitamin E, are potent inhibitors of cyclooxygenases. Proc. Natl. Acad. Sci. USA. 105:20464-20469.
  • Wagner, J.G., Jiang, Q., Harkema, J.R., Illek, B., Patel, D.D., Ames, B.N., and Peden, D.B. (2007) Ozone Enhancement of Lower Airway Allergic Inflammation is Prevented by Gamma-Tocopherol. Free Radical Biology & Medicine. 43(8):1176-88. Epub 2007 Jul 20.
  • Jiang, Q., Freiser, H., Wood, K.V., and Yin, X. (2007) Identification and quantitaion of novel vitamin E metabolites, sulfated long-chain carboxychromanols, in human A549 cells and in rats. J Lipid Res. 48:1221-30.

Books, Chapters & Monograph Publications

  • Moya, S. and Jiang, Q. (2011) The role of vitamin E forms in cancer prevention and therapy - Studies in human intervention trials and animal models. In: Nutraceuticals and Cancer. Sarkar, F.H Ed(s). Springer.
  • Jiang, Q. (2008) The metabolism of tocopherols and tocotrienols, and novel functions of their metabolites. In: Tocotrienols: Vitamin E beyond tocopherols. Watson, R.R Ed(s). Pp.309-329. Taylor and Francis Group, LLC.
  • Jiang, Q. (2006) Vitamin E forms as anti-inflammatory and anti-cancer agents by inhibiting cyclooxygenase mediated reactions and interrupting of sphingolipid synthesis. In: Encyclopedia of vitamin E. Preedy, V.R. and Watson, R.R Ed(s). Pp.785-796. CABI Publishing.


NUTR 43800 Micronutrient Metabolism
NUTR 60700 Nutritional Biochemistry and Physiology III
NUTR 63400 Nutrition and Cancer Prevention: This course provides an overview of the principles of cancer biology, identifies approaches to study the role of specific nutrients or bioactive compounds in molecular pathogenesis of cancer, and discusses existing research on the influences of dietary factors on cancer disease risk.
NUTR 69500 Seminar in Foods and Nutrition

Qing Jiang


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Fax: 765.494.0906
E-Mail: qjiang@purdue.edu

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