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Chicken plasma protein hydrolysate (CPPH) was prepared by trypsin with angiotensin I‐converting enzyme (ACE) inhibitory activity of 53.5% ± 0.14% and the degree of hydrolysis (DH) of 16.22% ± 0.21% at 1 mg·ml−1; then, five proteases, including pepsin, trypsin, papain, alcalase, and neutrase, were employed to improve ACE inhibitory ability by catalyzing plastein reaction. The results indicated that trypsin‐catalyzed plastein reaction showed the highest ACE inhibitory activity. The exogenous amino acids of leucine, histidine, tyrosine, valine, and cysteine were selected to modify the CPPH. The leucine‐modified plastein reaction released the highest ACE inhibitory activity. The effects of four reaction parameters on plastein reaction were studied, and the optimal conditions with the purpose of obtaining the most powerful ACE inhibitory peptides from modified products were obtained by response surface methodology (RSM). The maximum ACE inhibition rate of the modified hydrolysate reached 82.07% ± 0.03% prepared at concentration of hydrolysates of 30%, reaction time of 4.9 hr, pH value of 8.0, temperature of 40°C, and E/S ratio of 5,681.62 U·g−1. The results indicated that trypsin‐catalyzed plastein reaction increased ACE inhibitory activity of chicken plasma protein hydrolysates by 28.57%.

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This study reveals the therapeutic efficacy and mechanisms of action of the ginger species Halia Bara, or Zingiber officinale Roscoe var. rubrum (ZOR), on key immunopathogenic mechanisms relevant to psoriasis. It is known that psoriasis is a chronic autoimmune skin disease characterised by hyperplasia of epidermal keratinocytes and the accumulation of activated immune cells at sites of the disease. The disease is associated with aberrant activation of phagocytes (such as macrophages), Tlymphocytes and the production of pro-inflammatory cytokines and chemokines. In-depth experiments showed that ZOR chloroform extract (HB02), its active fraction (F6) and two identified compounds (6-shogaol and 1-dehydro-6-gingerdione) effectively inhibited nitric oxide (NO) and prostaglandin E 2 (PGE 2 ) production by activated macrophages. These effects were comparable to dexamethasone and indomethacin. More interestingly, ZOR samples at 20 µg/mL strongly down-regulated mRNA level of iNOS, IL-12p40 and IL-23p19 in pre-treatment experiments of activated macrophages. Further, studies of immune cell migration showed that F6 and the compounds inhibited the migration of polymorphonuclear neutrophils (PMNs) through human vascular endothelial cells (HUVEC) by influencing CD11b expression and CD62L shedding. In addition, F6 and the compounds were also shown to modulate activation of CD8 + cytotoxic T-lymphocytes as indicated by reduction of 'activation markers', CD25 and CD69 expression. An in vitro model of epidermal inflammation indicated that ZOR samples directly inhibited keratinocyte proliferation and the production of IL-20 and IL-8, both are key psoriasis-promoting cytokines. Hence, these experimental evidences substantiate the potential mechanisms of action of ZOR in ameliorating psoriasis.