In vivo anti-inflammatory and antinociceptive effects, and in vitro antioxidant, antiglycant and anti-neuroinflammatory actions of Syzygium malaccense

Abstract

Syzygium malaccense is popularly used to treat infl ammation and painrelated ailments. The species was assessed regarding its antioxidant, antiglycant, antiinfl ammatory, including anti-neuroinfl ammatory, and antinociceptive activities. Different models were employed to measure S. malaccense extract (ESM) antioxidant activity.The antiglycant activity was determined using the glucose-induced protein glycation model. LPS-induced neuroinfl ammation on murine BV-2 microglial cell line was used for anti-neuroinfl ammatory activity evaluation. The croton oil-induced ear edema test was accomplished to evaluate the in vivo anti-infl ammatory activity. Acetic acid-induced writhing together with formalin-induced paw licking assays were performed to evaluate the antinociceptive potential. Finally, the chemical characterization was accomplished by a UHPLC-MS analysis. ESM presented relevant antioxidant and antiglycant activity. NO production by BV-2 cells was reduced, indicating the relevant neuroprotective activity.ESM signifi cantly decreased the mice ear edema induced by croton oil and the nociceptive stimulus induced by acetic acid and formalin by central and peripheral mechanisms.The fl avonoids myricitrin, myricetin and quercetin were identifi ed and, as far as we know, the alkaloid reserpine was reported in the species for the fi rst time. The antioxidant and antiglycant potential of ESM, may be related to the in vivo anti-infl ammatory and antinociceptive effects, and to the in vitro neuroinfl ammation inhibition.

Roles of Syzygium in Anti-Cholinesterase, Anti-Diabetic, Anti-Inflammatory, and Antioxidant: From Alzheimer’s Perspective

“…S. malaccense leaf extract exerted neuroinflammatory protection against LPS-induced neuroinflammation on murine BV-2 microglial cell lines by reducing nitric oxide production [ 63 ]. Nitric oxide (NO) is one of the pro-inflammatory mediators released by microglia; reducing the NO levels can minimize immune outrage caused by microglia [ 4 ].…”