Astragaloside IV plays a role in reducing radiation-induced liver inflammation in mice by inhibiting thioredoxin-interacting protein/nod-like receptor protein 3 signaling pathway.

OBJECTIVE: To investigate the efficacy of Astragaloside IV (AS-IV) on radiation-induced liver inflammation in mice. METHODS: The mice were divided into normal group, dimethyl sulfoxide solvent group, irradiation group (IR), irradiation + AS-IV (20 mg/kg) group (IR+AS-20) and irradiation + AS-IV (40 mg/kg) group (IR+AS-40). One month after intraperitoneal injection of AS-IV, the mice were irradiated with 8Gry Co60γ, the blood was collected for biochemical analysis, and the liver was collected for hematoxylin-eosin staining, immunofluorescence and electron microscopic observation, oxidative stress, and Western blot analysis. RESULTS: The AS-IV treatment significantly ameliorated the pathological morphology of liver and reduced the alanine aminotransferase and aspertate amino-transferase levels in serum induced by radiation; AS-IV treatment also significantly reduced the expression of inflammatory factors tumor necrosis factor alpha and interleukin 6 and antagonized malonaldehyde content and superoxide dismutase activity in liver caused by radiation; in addition, AS-IV treatment can significantly inhibited the positive expression of thioredoxin-interacting protein (TXNIP) and nod-like receptor protein 3 (NLRP3) inflammasome in liver tissue after radiation; The expression of TXNIP, NLRP3 inflammasome, apoptosis-associated speck-like protein containing a CARD, cysteinyl aspartate-specific proteinase 1 and interleukin 1beta in the AS-IV prevention group decreased significantly compared to the radiation group. CONCLUSIONS: These findings suggested that Co60γ radiation can cause structural and functional damage to the liver, which may be related to the NLRP3 mediated inflammatory pathway; AS-IV may play a protective role by inhibiting the TXNIP/NLRP3 inflammasome signaling pathway in the radiation-induced liver injury model.

Distribution, function and regulation mechanism of aquaporin in the brain / 中国组织工程研究

BACKGROUND:The aquaporin (AQP), mainly AQP1, AQP4 and AQP9, are expressed in mammalian brain, while the others are sporadical y expressed. There is no evidence concerning the distribution, function and regulation mechanism of AQP in the brain. OBJECTIVE:To comprehensively analyze the research progress of the distribution, function and regulation mechanism of AQP in maintaining normal physiological function of the brain. METHODS:An online retrieval of PubMed database and CNKI database between January 1980 and July 2013 was performed for articles on the distribution, function and regulation mechanism of AQP, with the key words of“AQP1, AQP4, AQP9, function, brain, adjusting mechanism”in English and Chinese. A total of 163 papers were screened out and 85 of them met the inclusive criteria. RESULTS AND CONCLUSION:The existing studies about the expression, function and regulating mechanism of AQP1, AQP4 and AQP9 in the brain can be summarized as the fol owing three aspects: (1) AQP1 is expressed in the choroid plexus and participates in forming cerebrospinal fluid;in other types of cells, gas micromolecules CO 2 , NO, NH 3 and O 2 also cross through AQP1. (2) AQP4 is mainly expressed in the astrocytes, ependymal foot process and gelatin membranes, which can help the water in and out of the brain tissue, accelerate glial cellmigration and change neural activity. (3) AQP9 is mainly distributed in astrocytes and catecholamine neurons, the main function is involved in energy metabolism in the brain. Therefore, AQP is the key for water transport in the brain. Understanding the distribution, function and regulation mechanism of AQP wil play an important role in the treatment of brain diseases. The regulatory mechanism on the expression of AQPs in normal pathology and related disease remains unclear and related molecular signal pathway needs further exploration.