The main pathogenesis of Sjogren's syndrome was Yin Deficiency, dryness caused by blood stasis,dryness caused by dry poisoning, dryness caused by dampness, Qi deficiency, and incoordination of spleen and stomach,which led to damage of body fluid or transport barrier. Usually such factors were mutually intercross and interact, existing in the whole process of the disease. This is the important factor for a long course and intractable disease.

Uarthritis is a common inflammatory arthritis, which has been well known as the White Tiger arthritis in traditional Chinese medicine. This article discussed the pathogenesis of blood stasis and the related studies in hyperuricemia, acute and chronic phase of Uarthritis. It suggested that blood stasis is a crucial pathogeny of uarthritis. Thus, the chinese herb medicine of blood circulation drugs should beapplied in all the phases of Uarthritis.

Objective To study the influence of the Runzaoling on AQP1 and AQP5 in submaxillary gland of mice with Sjogren syndrome.Methods Sjogren syndrome mice models were setup by innducement method and divided into six groups randomly,including A group(blank group),B group(model group),C group (low dose group),D group(moderate dose group),E group(high dosage group)and F group(prednisone group).Immunohistochemical method was used to detect the of expressions of AQP1 and AQP5 of submaxillary gland in model mice.Result AQP1 expression showed:scattered flavescent particles were only found in submaxillary gland of group B and group C;AQP5 expression showed:brown-stained granules can be found in gland alveolous teleblem,lateral membrane,and basal lamina of submaxillary gland,secretory duct,and duct epithelia in B group mice;light brawn-stained granules can be found in group C mice;attenuated or disappear stained granules were found in acinus,secretory tube,and duct in D,E,and F group mice.Conclusion Runzaoling Can raise the expression of AQP5 in submaxillary gland of SS mice and increase the absorption quantity of water.

Objective To observe the spatiotemporal characteristics of the micro-structural injury in a rat model of diffuse axonal injury (DAI) and quantitatively assess the axonal injury severity in the vulnerable areas. Methods The 7.0 T MRI was performed in rats in DAI group (n =20) and control group ( n = 15 ) to synthesize the diffusion tensor imaging ( DTI) parameter map and calculate the parameter value of the vulnerable areas. Immunohistochemistry was used to detect β-APP expression in the vulnerable areas and the IPP software to quantitatively assess the axonal injury severity. Results Compared with the control group, FA and AD maps showed local signal defection or reduction in the corpus callosum and their values decreased significantly in the brain stem and corpus callosum in the DAI group (P ＜0.01 ). The integrated optical density (IOD) value of the vulnerable areas in the DAI group was significantly higher than that of the control group ( P ＜ 0. 01 ) , with the highest level in the brain stem (P＜0.05). The normalized FA, AD and ADC in the vulnerable areas were correlated negatively with the IOD (P ＜ 0.05). Conclusion DTI can detect invisible micro-structural injury in the vulnerable areas and quantitatively assess the axonal injury severity in vivo in the early stage.

ObjectlveTo evaluate the role of cannabinoid receptor 2 (CB2 receptor) in microglial injury induced by glutamate.MethodsMicroglia cells were randomly divided into 4 grups:control group (group C),microglial injury group ( group Ⅰ),specific CB2 receptor agonist AM 1241 group ( group AM1241 ) and specific CB2 receptor antagonist AM630 group (group AM630).In group C,the cells were cultured routinely for 26 h.In group Ⅰ,the cells were incubated in the culture medium containing glutamate 10 mmol/L for 24 h.In group AM1241,the cells were incubated in the culture medium containing AM1241 2 μmol/L for 2 h,and then in the culture medium containing glutamate 10 mmol/L for 24 h.In group AM630,the cells were incubated in the culture medium containing AM630 2 μmol/L for 2 h,and then in the culture medium containing glutamate 10 mmol/L for 24 h.The cell viability and release of LDH were measured.Microglial morphology was observed under microscope.Results Compared with group C,the cell viability was significantly decreased,and the release of LDH was significantly increased in groups Ⅰ,AM1241 and AM630 (P ＜ 0.05).Compared with group Ⅰ,the cell viability was significantly increased,and the release of LDH was significantly decreased in group AM1241 ( P ＜ 0.05).There was no significant difference in the cell viability and the release of LDH between groups 1 and AM630 ( P ＞ 0.05).Conclusion Glutamate induces microglial injury through inhibiting the function of CB2 receptor.

Primary Sj?gren's syndrome(pSS)is a chronic inflammatory autoimmune disease involving a variety of exocrine glands.It is a common autoimmune disease in the department of rheumatology.However,the pathogenesis of pSS is still unclear,re-sulting in lack of treatment.While the international research on pSS is also increasing,we review the latest literature on the mecha-nism of Sj?gren's syndrome under different factors.In this paper,the process mechanism of Sj?gren's syndrome is summarized from the aspects of heredity,environment,autoimmune cells and autoantibodies.