Gallic Acid-L-Leucine Conjugate Protects Mice against LPS-Induced Inflammation and Sepsis via Correcting Proinflammatory Lipid Mediator Profiles and Oxidative Stress

Figure 4

In vivo effects of GAL on the survival of mice against LPS-induced toxicity. (a) Experimental design. Mice were treated with GAL, dexamethasone (DMS), or vehicle via i.p. injection for 3 days. On day 3, LPS or 0.9% NaCl saline was administrated via i.p. injection at 12 h after GAL injection. (b) Animal survival. Mice were randomly divided into three groups (): control, receiving vehicle; LPS, receiving 25 mg/kg LPS only; and LPS + GAL, receiving three injections of 5 mg/kg GAL and a single injection of 25 mg/kg LPS. Animal survival was monitored every 12 h for 10 days. (c) Measurement of body weight and spleen size. Following a 10-day treatment, mice were weighed and sacrificed. Spleens were collected, weighed, and imaged. (LPS versus control); (GAL + LPS versus LPS). (d) Protein expression levels of iNOS and COX-2 in residential peritoneal macrophages. Residential peritoneal macrophages were isolated and analyzed for iNOS and COX-2 levels by Western blotting. Data represent mean ± SD of three animals per group. and (GAL + LPS versus LPS alone). (e) Protein expression levels of iNOS and COX-2 in spleens. Spleen tissues were recovered and analyzed for iNOS and COX-2 levels by Western blotting. Data represent mean ± SD of three animals per group. and (GAL + LPS, DMS + LPS versus LPS alone). DMS: dexamethasone. (f) Plasma levels of proinflammatory lipid mediators. Lipid mediators were purified from plasma samples and quantified by LC-MS/MS technique. Data represent mean ± SD of three animals per group. and (GAL + LPS versus LPS).

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