The podocyte, a type of glomerular epithelial cell, is the key constituent of the filtration barrier layer in the kidney. Previous studies have shown that long non‑coding RNA (lncRNA)‑taurine‑upregulated gene 1 (TUG1) served a protective role in diabetes‑induced podocyte damage. The aim of the present study was to investigate the potential role of TUG1 in the progress of podocyte injury induced by lipopolysaccharide (LPS), and explore the underlying mechanisms. The results showed that TUG1 expression was suppressed in LPS‑induced podocytes. Enhanced TUG1 expression by exogenous recombinant vector regulated the expression of podocyte associated proteins [Nephrin, Podocin and CCAAT/enhancer‑binding protein (CHOP)]. A marked decrease was observed in the level the albumin influx in cells transfected with TUG1. Further study indicated that microRNA (miR)‑197 is a potential target of TUG1. The enhanced level of miR‑197 induced by LPS was inhibited in cells transfected with TUG1. The decreased Nephrin and Podocin expression, upregulated CHOP expression and the increased albumin influx were slightly enhanced by miR‑197 mimic transfection, while markedly suppressed by miR‑197 inhibitor transfection in LPS‑induced podocytes. Mitogen‑activated protein kinase (MAPK) protein was predicted as a potential target of miR‑197. The downregulated expression of phosphorylated‑MAPK/MAPK induced by LPS was significantly suppressed by TUG1 transfection in podocytes. In addition to this, autophagy was promoted by TUG1 transfection via the elevation of the Beclin1 and light chain (LC)3 II/LC3 I levels, and suppressing p62 expression. However, the p38 MAPK inhibitor SB203580 reversed the changes that TUG1 induced in the levels of Beclin1, LC3 II/LC3 I and p62. Taken together, these results demonstrated that LPS‑induced podocyte injury could be alleviated by the TUG1/miR‑197/MAPK1 axis.