The Lectin fromRaddi Leaves (SteLL) Exhibited Anti-Inflammatory Activity in Lipopolysaccharide-Induced Acute Lung Injury in Mice.

Abstract

Acute lung injury (ALI) is a severe inflammatory condition associated with high morbidity and mortality, and there are currently no specific pharmacological treatments available. In this context, plants and natural products have emerged as promising therapeutic alternatives. SteLL (Raddi leaf lectin) has demonstrated several biological activities, including anti-inflammatory and immunomodulatory effects. This study evaluated the anti-inflammatory effects of SteLL in a murine model of lipopolysaccharide (LPS)-induced ALI. Female BALB/c mice received intraperitoneal (i.p.) administration of SteLL (1, 5, or 10 mg/kg), dexamethasone (2 mg/kg), or vehicle (PBS). Sixty minutes later, ALI was induced by intranasal instillation of 25 µL of LPS (1 μg/μL). After 24 h, the animals were euthanized. Bronchoalveolar lavage fluid (BALF) was obtained to evaluate inflammatory parameters and lungs were collected for histopathological analysis. The tested doses of SteLL resulted in a 45-66% lower leukocyte infiltration. The group treated with 5 mg/kg exhibited a lower proportion of neutrophils and a higher proportion of mononucleated cells. Pre-treatment with SteLL also minimized plasma leakage and myeloperoxidase (MPO) activity. Furthermore, SteLL attenuated the release of pro-inflammatory cytokines at all tested doses as well as prevented nitric oxide (NO) production at the highest dose (10 mg/kg). Histopathological analysis showed that SteLL (5 and 10 mg/kg) attenuated LPS-induced lung injury. Overall, SteLL demonstrated significant anti-inflammatory effects, showing its potential as a plant-derived compound for modulating pulmonary inflammation.