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TWP is widely used in clinical autoimmune diseases and effective. Meanwhile, its toxic side effects have gradually taken by the people. This study aimed to: 1. Explore TWP immunotoxicity management roles, from \(2) evaluate TWP immune effects of Pharmacology and Toxicology common mechanism for the clinical TWP provide experimental evidence for a reasonable application. Experimental study of the SD rats were selected as experimental subjects, the rats were randomly divided into eight groups: control D1, D2 group, low, medium and high dose groups, low, medium and high dose recovery group. 3 weeks after oral administration, the first detected on the immune system (immune organs, immune cells) of. The results showed that: Compared with control group, low dose group (clinically equivalent dose) spleen index, NK cell activity, T, B lymphocyte proliferation and transformation function changes are not obvious (P> 0.05), thymus index decreased significantly (P <0.05 ); middle dose group spleen index, thymus index, NK cell activity, B lymphocyte proliferation and transformation capabilities were significantly decreased (P <0.05), T lymphocyte proliferation and transformation capacity significantly decreased (P <0.01); spleen index high dose group, B lymphocyte proliferation and transformation capacity decreased significantly (P <0.05), thymus index, NK cell activity, T lymphocyte proliferation and transformation capacity significantly decreased (P <0.01): withdrawal two weeks after the high-dose group only thymus index did not recover (P <0.05). The liver is the main research topics selected objects from the cellular and molecular level to explore its damage and immunotoxicity TWP correlation. Experimental results show that: compared with the control group, low dose group index liver, kidney index, ALT, ALP, AST, CREA, UREA and UA tended to increase, but not statistically significant (P> 0.05); medium dose liver index increased significantly (P <0.01), kidney index, AST, ALT, ALP, CREA increased significantly (P <0.05), UREA, UA tended to increase, but not statistically significant (P> 0.05); liver high dose group index, kidney index increased significantly (P <0.05), ALT, ALP, AST, CREA, UREA, and UA increased significantly (P <0.01). Two weeks after drug withdrawal, middle dose group liver index, kidney index, ALT, ALP, AST, CREA, UREA and UA fully restored; values ??above the high dose group was no complete recovery (P <0.05). Immunohistochemical detection of rat liver Kupffer cell surface markers CD 68 activation of renal tubular epithelial cells in CD 40 expression, liver and kidney tissue of Fas apoptosis gene expression; ELISA determination of rat liver homogenates TNF-α levels, flow cytometry apoptosis of rat hepatocytes. The results showed that: compared with the control group, low-dose group and kidney tissue expression of Fas, renal tubular epithelial cells CD 40 expression and liver tissue homogenate TNF-α content change was not statistically significant ( P> 0.05), hepatic Kupffer cells CD 68 expression of hepatocyte apoptosis rate increased significantly (P <0.05); dose group hepatocyte apoptosis and liver CD 68 < / sub> expression increased significantly (P <0.01), liver and kidney tissue expression of Fas, renal tubular epithelial cells CD 40 expression and liver tissue homogenate TNF-α levels were increased significantly (P < 0.05); high-dose group, these indicators were increased significantly (P <0.01). Histopathological results showed that: the low-dose group showed hepatocytes, renal tubular epithelial cell morphology was normal, occasional scattered interstitial inflammatory cell infiltration: middle dose group showed liver and kidney tissue structure is unclear, cell swelling, degeneration obvious, liver punctate necrotic cells can be seen, fatty degeneration: high-dose group showed liver cells, lysis and necrosis of renal tubular epithelial cell edema, organizational structure disorder. Withdrawal two weeks after the middle dose group, these changes return to normal, high-dose liver, kidney injury did not recover. The results showed that: GTW experimental animals immune system and its function has a certain inhibition certain aspects, was a certain \Meanwhile, TWP has liver injury in rats, was positively correlated with the dose. This damage in the two weeks after discontinuation of low, middle dose group is reversible; higher doses irreversible. Tip GTW induced liver and kidney damage and immunotoxicity TWP may have some relevance. Its possible immunotoxicity management mechanism is as follows: TWP some of the ingredients contained in the liver and kidney Neijing metabolic conversion of pro-electronic-based, free radicals and groups, and covalent binding of macromolecules or cause lipid peroxidation cause liver cell necrosis. Necrosis of the liver cells can be stimulated, and liver and kidney tissue macrophages, leading to TNF-α synthesis and secretion, increased liver and kidney tissue damage: and raised liver cells, Fas expression in renal tubular epithelial cells, possibly through Fas pathway induction of apoptosis leading to liver and kidney damage; also allows lymphocytes and other inflammatory cells to migrate to areas of damage, initiating a series of autoimmune inflammatory injury.
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