Abstract:
Objective To assess the therapeutic effect of sodium tanshinone ⅡA sulfonate on early-stage silicosis in rats.
Methods Ninety-six adult male SD rats of SPF grade were randomly divided into normal control group, drug control group, dynamic dust exposure group, and drug treatment group, and sacrificed at designed time points (7 d, 14 d, 28 d, and 56 d), with six rats in each subgroup. The dust exposure group was given dynamic inhalation of silica dust; the drug treatment group received intraperitoneal injection of sodium tanshinone ⅡA sulfonate at 15 mg/(kg·d) in addition to dust exposure everyday; the drug control group was only given an equal dose of sodium tanshinone ⅡA sulfonate; the normal control group received neither dust exposure nor designed treatment. The pathological changes of lung tissues were observed by hematoxylin-eosin (HE) staining; lymphatic hyperplasia in lung tissues was detected by immunohistochemistry after lymphatic vessels being labeled with hyaluronic acid receptor 1 (LYVE-1); malondialdehyde (MDA) in rat lymph was assessed by biochemical kit; laminin (LN) in serum was evaluated by enzymelinked immunosorbent assay; and the expression of monocyte chemotactic protein-1 (MCP-1) in rat lung tissues was detected by Western blot.
Results The HE staining results showed that the pathological changes in the rats of the drug treatment group were relieved compared with those of the dynamic dust exposure group.Compared with the normal control group, the MDA content and LYVE-1 labeled positive lymphatic vessels in lymph of rats exposed to dynamic dust reached the peak at 14 d(10.61±0.56)μg/L, 4.50 (4.00-5.00); the levels of MCP-1 in lung tissues and LN in serum of rats exposed to dynamic dust were 1.84±0.01 and (456.73±10.01)μg/L at 56 d. Compared with the dynamic dust exposure group at 56d, the levels of MDA in lymph(5.69±0.90)μg/L, MCP-1 in lung tissues (1.45±0.07), and LN in serum(427.43±13.89)μg/L of the drug treatment group were decreased.
Conclusion Sodium tanshinone ⅡA sulfonate injection may delay the pathogenesis of silicosis in rats by improving the microcirculation of lung lymph, oxidative stress, and inflammatory reaction.
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