Objective To investigate the mechanism of allicin in improving human peritoneal mesenchymal cellmesenchymal transformation induced by high glucose. Methods Human peritoneal mesothelial cells (HPMCs) were divided into the following groups. Group 1: ①Control group; ②8. 5 mmol/ L D-glucose group (8. 5 mmol/ L DG group); ③17 mmol/ L D-glucose group (17 mmol/ L DG group); ④34 mmol/ L D-glucose group (34 mmol/ L DG group); ⑤68 mmol/ L D-glucose group (68 mmol/ L DG group). Except in the control group, the groups were treated with the corresponding concentrations of D-glucose for 48 h. Group 2: ①Control group; ②34 mmol/ L D-glucose group (HG group); ③34 mmol/ L D-glucose + low dose allicin group (AL-L group); ④34 mmol/ L D-glucose + medium dose allicin group (AL-M group); ⑤34 mmol/ L glucose + high-dose allicin group (AL-H group); ⑥34 mmol/ L D-glucose + JAK2 inhibitor group (JAK2 group). The HG group was treated with 34 mmol/ L D-glucose for 48 h. AL-L, AL-M and AL-H groups were pretreated with 34 mmol/ L D-glucose for 6 h and then treated with 10, 20 and 40 ng/ mL allicin for 48 h, respectively. The JAK2 group was pretreated with 1 μmol/ L AG490 for 6 h and then treated with 34 mmol/ L D-glucose for 48 h. IL-6, TNF-α, and IL-1β contents in HPMC culture supernatants were determined by ELISA. A CCK-8 assay was used to assess cell proliferation and morphology. JAK2, p-JAK2, STAT3, p-STAT3, N-cadherin, E-cadherin, Vimentin, α-SMA, MCP-1, p65 and p-p65 protein expression was detected by Western blot. Results Compared with the control group, the relative survival rate of HPMCs in the high glucose induced group was significantly reduced (P<0. 01), cell morphology was abnormal, expression of α-SMA, N-cadherin and Vimentin that promote epithelial-mesenchymal transition was significantly upregulated, and expression of E-cadherin, which inhibits EMT, was significantly downregulated. The JAK2/ STAT3 signaling pathway was activated, leading to EMT ( P< 0. 01). Allicin significantly promoted HPMC proliferation induced by high glucose, reversed the abnormal cell morphology, regulated the expression of EMT-related proteins, and improved epithelial-mesenchymal transition of HPMCs. Compared with the high glucose group, proinflammatory cytokines IL-1β, IL-6 and TNF-α in HPMCs in the allicin treatment group were significantly decreased and expression of proinflammatory proteins p-p50 and MCP1 was significantly downregulated, indicating that allicin improved the inflammation caused by EMT. Conclusions Allicin improved EMT and inflammation induced by high glucose by inhibiting the JAK2/ STAT3 signaling pathway to regulate the expression EMT markers, inflammatory signaling proteins, and proinflammatory factors.