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Protective effect of ginsenoside Rd on lipopolysaccharide-induced acute lung injury through its anti-inflammatory and anti-oxidative activity

1 Department of Pharmacy, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China
2 Guangzhou Darui Biotechnology Co., Ltd., Guangzhou, China
3 Obstetrics and Gynecology, Shenzhen Longhua District Central Hospital, Shenzhen, China
4 Medical Laboratory, Shenzhen Longhua District Central Hospital, Shenzhen, China
5 Department of Clinical Laboratory Medicine, Guangdong Second Provincial General Hospital, Guangzhou, China
6 College of pharmacy, Jinan University, Guangzhou, China

Correspondence Address:
Yong-Li Situ,
601 Huangpu Avenue West, Guangzhou City, Postal Code: 510632, Guangdong Province
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/wjtcm.wjtcm_38_21

Background: Inflammation and oxidation stress are key factors in the mechanism of acute lung injury (ALI). Therefore, suppression of the inflammatory response and oxidative stress could be a potential strategy to treat lipopolysaccharide (LPS)-induced ALI. Ginsenoside Rd (Rd), a natural Ginseng extract, alleviates inflammation and oxidative stress in several diseases such as Alzheimer's disease and cerebral ischemia, but its effect on ALI is still unclear. Aims and Objectives: To explore the protective effect of Rd on LPS-induced ALI and explored associated mechanisms. Materials and Methods: Mice were divided into five groups: A sham-operated group, a LPS-induced ALI group, and three LPS groups pretreated with Rd doses of 20, 40, and 80 mg/kg, respectively. The pathological changes of lung, collagen deposition, pulmonary edema, inflammatory cytokine, oxidative stress and the expression levels of TLR4 and NF-κB were detected. Results: The oral administration of Rd dose dependently attenuated histopathologic changes in the lung, lung edema, pulmonary collagen deposition, protein concentration in bronchoalveolar lavage fluid (BALF), myeloperoxidase (MPO) activity, and inflammatory cell infiltration. In addition, Rd suppressed the LPS-induced inflammatory cytokines tumor necrosis factor-α, interleukin (IL)-6, and IL-1 β in BALF. The productions of oxidative stress-related enzymes (catalase, superoxide dismutase, and glutathione peroxidase) in lung tissue were significantly upregulated by Rd administration. However, malondialdehyde and pulmonary MPO activity was reduced in the Rd-pretreated groups when compared with LPS-induced ALI group. Rd treatment also dose dependently suppressed LPS-induced NF-κB activation and TLR4 expression. Conclusion: Overall, these findings provide evidence that Rd pretreatment inhibits LPS-induced ALI through anti-inflammatory and antioxidative actions, suggesting that it could be a promising protective drug for LPS-induced ALI.

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