α-Linolenic Acid (ALA) is an essential fatty acid that cannot be synthesized by the human body and is obtained by isolating it from seed oils. α-Linolenic acid has been shown to improve memory, inhibit thrombosis, and lower blood lipids.

METHODS: Osteosarcoma cells MG63, 143B and U2OS were treated with α-Linolenic Acid (10-200 µM) for 24 h. Cell viability was determined by MTT assay.
RESULTS: α-Linolenic Acid showed a highly inhibitory effect on cell proliferation in a dose-dependent manner, with IC50 values of 51.69±0.14 µM in MG63 cells, 56.93±0.23 µM in 143B cells and 49.8±0.50 µM in U2OS cells.[1]
METHODS: Breast cancer cells MDA-MB-231 and MCF-7 were treated with α-Linolenic Acid (25-100 µM) for 24 h. Apoptosis was detected by flow cytometer.
RESULTS: The percentage of apoptotic cells in the early (from 2.9% to 23.5% and from 5.5% to 16.7%, respectively) and late (from 0.6% to 3.4% and from 2.0% to 13.8%, respectively) apoptotic stages was significantly increased in MDA-MB-231 and MCF-7 cells treated with 100 µM α-Linolenic Acid. percentage significantly increased, which was significantly higher compared to untreated control cells. [2]

METHODS: To study the therapeutic effect on colitis in mice, α-Linolenic Acid (150-300 mg/kg, dispersed in 0.25% Tween-20) was administered by gavage to HFHSD-fed BABL/c mice once daily for nine weeks. At the end of nine weeks, experimental colitis was induced by intracolonic injection of TNBS.
RESULTS: Low α-Linolenic Acid administration significantly ameliorated TNBS-induced clinical manifestations, body weight loss, spleen weight loss, and histologic damage. In contrast, high α-Linolenic Acid administration did not improve colitis and even exacerbated symptoms.HFHSD exacerbated TNBS-induced colitis via the Th1/Th17 pathway. Low α-Linolenic Acid showed a protective effect against TNBS-induced colitis via the Th1/Th2/Th17 pathway. [3]