Infammopharmacology 16 (2008) 188–194 0925-4692/08/040188-7 DOI 10.1007/s10787-008-8010-2 © Birkhäuser Verlag, Basel, 2008 Inflammopharmacology Abstract. The lipid extract of Perna canaliculus (Lyprinol  ) has known anti-infammatory effects. However, the only in- formation on mechanisms is regulation of cytokine secretion. Therefore, we conducted a proteomic study exploring the ef- fects of Lyprinol on protein expression in splenocytes collect- ed from AIA rats. Splenocytes from AIA rats fed with Lypri- nol had increased protein expression of malate dehydrogenase (MDH). Lyprinol also decreased the expressions of 5 other proteins: protein-o-mannosyl- transferase 2 (PMT-2), Tdrd 7, telethonin, dynactin 2 and protein disulfde isomerase (PDI or glucose-regulated protein (GRP)). Besides MDH, PMT- 2, titin-cap protein and protein disulfde isomerase (PDI) are known to be related to metabolism. However, it is currently unknown if Lyprinol administration decreases metabolic glu- cose in the body and alleviates symptoms of infammation and arthritis. Further experiments are required to correlate levels of citric acid intermediates and glucose to the severity of in- fammation and pain in AIA rats fed Lyprinol. Key words: Lyprinol – Adjuvant-induced arthritis – Proteom- ics – Malate dehydrogenase – Protein disulfde isomerase – Protein-o-mannoyl-transferase – Titin-cap protein – Tdrd7 protein Introduction Freeze-dried powdered preparations of whole (i. e. without shell) green-lipped mussel (Perna canaliculus) from New Zealand given orally to rats were shown to have some mod- est anti-infammatory activity (carrageenan paw oedema in rats) (Rainsford and Whitehouse, 1980). After the frst report, validation experiments by another group found that the crude extract was not effective when given orally (Miller and Orm- Research Article Differential protein expression induced by a lipid extract of Perna canaliculus in splenocytes of rats with adjuvant-induced arthritis C.-H. Lee, Y. K.-C. Butt, M.-S. Wong and S. C.-L. Lo * Department of Applied Biology and Chemical Technology, The Hong Kong Polytechnic University, Hung Hom, Kowloon, Hong Kong SAR, China and State Key Laboratory of Chinese Medicine and Molecular Pharmacology, Shenzhen, China, Fax: ++852 23649932, e-mail: bcsamlo@inet.polyu.edu.hk Received 14 May 2008; accepted 19 June 2008 rod, 1980). Improvements on the preparation process were made subsequently. Eventually, a lipid-rich fraction prepared by supercritical fuid [CO 2 ] extraction of the freeze-dried stabilized green-lipped mussel Perna canaliculus powder (Lyprinol ® ) was prepared. When given orally, it was reported to have signifcant anti-infammatory activity (Whitehouse et al., 1997). Similar anti-infammatory effects were found in other disease models and in humans (Emelyanov et al., 2002, Halpern, 2000, Shiels and Whitehouse, 2000, Tenikoff et al., 2005, Yuan et al., 2006). This lipid-rich fraction was found to contain fve main lipid classes including sterol es- ters, triglycerides, free fatty acids, sterols and polar lipids (Murphy et al., 2002, Wolyniak et al., 2005). There are 90 component fatty acids in this extract while omega-3 polyun- saturated fatty acids (PUFA) are the most abundant PUFAs. Further, eicosapentaenoic acid (EPA, 20:5 omega-3) and docosahexaenoic acid (DHA, 22:6 omega-3) are the major omega-3 PUFAs present in this extract (Murphy et al., 2002, Wolyniak et al., 2005). Most Western diets provide a surplus amount of omega-6 PUFAs that become part of our cellular membranes and render them prone to induction of infam- matory processes and chronic diseases (De Lorgeril, 2007, Simopoulos, 2006). The bodily infammation processes are usually initiated in the phospholipids of the cell membrane. Arachidonic acid can either (1) go through the 5-lipoxyge- nase pathway to produce leukotrienes or (2) go through the cyclo-oxygenase pathway to produce prostaglandins and thromboxane A2 (Gonzalez-Periz and Claria, 2007). In the 5-lipoxygenase pathway, arachidonic acid is converted into 5-HPETE by 5-lipo-oxygenase to form leukotriene A 4 and 5 HETE; subsequently, leukotriene A4 is converted to LTB 4 (leukotriene B 4 ) by LTA 4 hydrolase, or to LTC 4 (leukotriene C4) by LTC 4 synthase leukotriene B 4 (LTB 4 ) (Murphy and Gijon, 2007). In an earlier study on the mechanism of ac- tion of Lyprinol, it was found that Lyprinol reduced the in- terleukin-4 induced LTB 4 production by human monocytes * Corresponding author