Cedrol ameliorates lipopolysaccharide-induced systemic inflammation and lung injury in rats

Cedrol is sesquiterpene alcohol with anti-inflammatory and antioxidant properties; this study evaluated cedrol protective effects against lipopolysaccharide (LPS)-induced systemic inflammation and lung damage. Forty male rats were randomized into the following groups: control (saline); LPS (1 mg/kg); and LPS + cedrol 7.5, 15, and 30 mg/kg. Cedrol was administered for 2 weeks (day 1-14, once daily, orally) while LPS was injected on days 8-14 (once daily, intraperitoneally). Finally, blood, bronchoalveolar lavage fluid (BALF) and lung tissue samples were obtained. White blood cells (WBC) counts, tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, oxidative stress markers, and nitric oxide (NO) levels were determined, and lung histopathological changes were evaluated. LPS significantly increased total WBC, neutrophil and monocyte counts, and the levels of TNF-α, IL-1β and malondialdehyde (MDA), while significantly reduced total thiol content, and catalase (CAT) and superoxide dismutase (SOD) activity in serum compared to the control group. The highest dose of cedrol significantly reduced total WBC, neutrophil, lymphocyte, and monocyte counts, downregulated the levels of TNF-α, IL-1β and MDA, but increased total thiol content, and CAT and SOD activity, compared to the LPS group. In the lung, LPS induced histopathological injury, and it significantly increased BALF total and differential WBC counts and TNF-α, NO, and MDA levels, while reducing thiol content, and CAT and SOD activity, compared to the control group; cedrol dose-dependently reversed all these changes. It is concluded that cedrol dose-dependently ameliorated LPS-induced systemic and lung inflammation and oxidative stress.