This work aimed to assess anti-inflammatory and related properties of a phospholipid mixture purified from porcine lung tissues, named KT&G101, which is being developed as a novel topical remedy for atopic dermatitis. KT&G101 consists of pure phospholipids, mainly phosphatidylcholine (PC) and other phospholipids such as phosphatidylinositol (PI) and phosphatidylserine (PS). Its predominant PC species is 1,2-dipalmitoylphosphatidylcholine (DPPC). KT&G101 exhibited an anti-angiogenic activity in the chick chorioallantoic membrane (CAM) assay. Oral administration of KT&G101 at the dosages of 100, 200 and 400 mg/kg body weight gave rise to an inhibition of 15.4%, 25.3% and 30.1% in the vascular permeability assay, respectively. In the carrageenan-induced inflammation in the air pouches, KT&G101 significantly diminished the volume of exudates in the pouches, the number of polymorphonuclear leukocytes and nitrite content in exudates. In the acetic acid-induced writhing response, oral administration of KT&G101 at the dosages of 50, 100 and 200 mg/kg body weight showed the reduction of 21.6%, 51.6% and 60.8% in the pain response of mice, respectively. It was also able to diminish the nitric oxide (NO) and reactive oxygen species (ROS) levels in the lipopolysaccharide (LPS)-stimulated RAW264.7 macrophage cells. KT&G101 displayed a significant suppression on the induction of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in the stimulated RAW264.7 cells. However, the free radical scavenging activity of KT&G101 was detected to be very weak in the 1,1-diphenyl-2-picrylhydrazyl (DPPH) assay. Taken together, KT&G101 possesses anti-inflammatory and related antinociceptive and anti-angiogenic activities, which indirectly supports its use as an anti-atopic therapy.

The first gene encoding gamma-glutamyl transpeptidase (GGTI) of the fission yeast has previously been characterized, and its expression was found to be regulated by various oxidative stress-inducing agents. In this work, a second gene, encoding GGTII, was cloned and characterized from the fission yeast Schizosaccharomyces pombe. The structural gene encoding GGTII was amplified from the genomic DNA of the fission yeast and ligated into the shuttle vector pRS316 to generate the recombinant plasmid pPHJ02. The determined sequence contains 3040 bp and is able to encode the putative 611 amino acid sequence of GGTII, which resembles the counterparts of Saccharomyces cerevisiae, Homo sapiens, Rattus norvegicus, and Escherichia coli. The DNA sequence also contains 940-bp upstream and 289-bp downstream regions of the GGTII gene. The Schizosaccharomyces pombe cells harboring plasmid pPHJ02 showed about 4-fold higher GGT activity in the exponential phase than the cells harboring the vector only, indicating that the cloned GGTII gene is functional. The S. pombe cells containing the cloned GGTII gene were found to contain higher levels of both intracellular glutathione (GSH) content and GSH uptake. The S. pombe cells harboring plasmid pPHJ02 showed increased survival on solid media containing hydrogen peroxide, diethylmaleate, aluminum chloride, cadmium chloride, or mercuric chloride. The GGTII mRNA level was significantly elevated by treatment with GSH-depleting diethylmaleate. These results imply that the S. pombe GGTII gene produces functional GGTII protein and is involved in the response to oxidative stresses in S. pombe cells.

The total phospholipid fraction (TPF) has anti-inflammatory properties and reduces apoptosis in animal models. Our objective was to assess the effects of TPF on pressure ulcers in a mouse model of cutaneous ischemic-reperfusion (I/R) injury. Cutaneous I/R injury was created by trapping the dorsal skin between two magnetic disks for 12 h, followed by disk removal. TPF administration in I/R areas at the beginning of reperfusion significantly inhibited the formation of pressure ulcers. The number of neutrophils and M1 macrophages and the levels of proinflammatory mediators MCP-1, IL-1β, IL-6, and TNF-α in the wound area were reduced upon TPF treatment. Collagen synthesis and α-SMA-positive microvessel density significantly increased in the wounds of TPF-treated mice. Additionally, TPF inhibited cutaneous I/R injury-induced formation and accumulation of apoptotic cells. Moreover, TPF increased the expression of filaggrin and involucrin. In conclusion, TPF may inhibit cutaneous I/R injury-induced formation of pressure ulcers by regulating inflammation, collagen production, angiogenesis, and skin barrier restoration. Therefore, exogenous application of TPF might have therapeutic potential with respect to cutaneous I/R injuries like decubitus ulcers.