Cytokine production induced by marine algae lectins in BALB/c mice splenocytes.

Marine algae can serve as sources of bioactive compounds and currently have been shown their potential biological and pharmaceutical applications. Marine algae lectins have been shown to be effective at controlling inflammatory processes. This work aimed to analyze the immunostimulatory properties of lectins from the marine algae Solieria filiformis (SfL), Pterocladiella capillacea (PcL) and Caulerpa cupressoides (CcL). This analysis was performed on BALB/c mouse splenocytes by measuring cytokine and nitric oxide production and cellular damage using tests of cytotoxicity and cell viability. These lectins were not cytotoxic (1-100 µg/mL), and were not able to induce IFN-γ and IL-2 production. IL- 10 production was induced at high levels by all lectins tested. Treatment with SfL induced IL-6 production at higher levels at all experimental times, whereas treatment with PcL and CcL induced higher levels only in 24 and 72 h. Treatment with SfL did not result in nitrite oxide production, whereas treatment with PcL or CcL was able to induce nitrite release at high levels (after 24, 48 and 72 h). Lesser cellular damage (5%) was observed in splenocytes treated with these lectins (10 µg/mL). Thus, the lectins from these algae were not cytotoxic, promoted increased in cell viability and induced Th2 immune responses in mouse splenocytes, indicating that they have anti-inflammatory effects.

Antinociceptive and anti-inflammatory activities of lectin from the marine green alga Caulerpa cupressoides.

The search for new compounds for controlling pain and inflammation, with minimal side effects has focused on marine algae. The aim of this work was to investigate the effect of the purified lectin from the green marine alga Caulerpa cupressoides (CcL) in classical models of nociception and inflammation. Male Swiss mice received i.v. CcL 30 min prior to receiving 0.8% acetic acid (10 ml/kg; i.p); 1% formalin (20 microl; s.c.) or were subjected to thermal stimuli. We observed that CcL (3, 9 or 27 mg/kg) significantly reduced the number of writhes induced by acetic acid by 37.2%; 53.5% and 86.0%, respectively. CcL (27 mg/kg) also reduced the second phase of the formalin test. However, CcL (27 mg/kg) did not present significant antinociceptive effects in the hot plate test, when compared to morphine, suggesting that its antinociceptive action occurs predominantly through a peripheral mechanism. The antinociceptive effects were abolished when CcL was pre-incubated with mucin (20mg/kg; i.v.). When CcL (9 mg/kg) was administered i.v. in Wistar rats 30 min before carrageenan administration, neutrophil counts were reduced by 65.9%. CcL also inhibited paw edema in all time intervals, especially at the third hour. Finally, CcL (9 mg/kg) administered i.v. in mice did not cause hepatic or renal alterations and did not affect body mass or macroscopy of the organs examined. In conclusion, CcL appears to have important antinociceptive and anti-inflammatory activities and could represent an important agent for future studies.