AIM:To explore the production and cytotoxicity of the reactive oxygen species(ROS)induced by diallyl trisulfide(DATS)in HL-60 cells.METHODS:HL-60 cells were either treated with various doses of DATS alone,or DATS combination with apocynin,a specific NADPH oxidase inhibitor,or with antioxidant N-acetyl-L-cysteine(NAC)for 0,1,3,6,12 and 24 h,respectively.The intracellular ROS level was measured by flow cytometry.The activity of NADPH oxidase was evaluated by NBT reduction experiment.The content of both malondialdehyde(MDA)and the protein carbonyl were analyzed by spectrophotometer.RESULTS:The results from flow cytometry indicated that DATS significantly increased the intracellular ROS level in HL-60 cells(P

[Objective]To discuss the diagnosis and treatment of lumbar disc herniation from the theory of kidney governor Qi pulse founded by Professor LYU Lijiang.[Methods]Firstly,analyze the relationship among the kidneys,the Governing Vessel and the spine,clarify the roles of the kidneys and the Governing Vessel on the spine,and understand the theoretical basis of the theory of kidney governor Qi pulse.Then the etiology and pathogenesis of lumbar disc herniation were analyzed based on the theory of kidney governor Qi pulse.Finally,the treatment principles of lumbar disc herniation were analyzed from different treatment methods.[Results]The three elements of kidney-Governing Vessel-spine are closely related to each other.The fundamental pathogenesis of lumbar disc herniation lies in the deficiency of the kidney and stagnation of Governing Vessel.Deficiency of the kidney results in emptiness of Governing Vessel,while Governing Vessel stagnation leads to a dysfunction in the ascending and descending of Yin and Yang in Governing Vessel.This disruption causes an inadequate circulation of Qi,blood,essence and body fluids,leading to a lack of nourishment for the tendons and bones and an obstruction in the flow of Qi and vessels.The treatment principle is to benefit the kidney and pass the Governing Vessel.By supplementing and tonifying the kidney Qi and replenishing the kidney essence,the Governing Vessel becomes filled,allowing the ascent of Governing Vessel Yang Qi and the descent of Governing Vessel Yin Qi.This facilitates the transformation of essence and marrow,promoting the smooth circulation of Qi,blood,essence and body fluids.Consequently,the lumbar vertebrae becomes stable,the lumbar muscles strengthen,the meridians and collaterals regulate properly,and the flow of Qi and vessels becomes unobstructed.[Conclusion]The theory of kidney governor Qi pulse can guide the clinical diagnosis and treatment of lumbar disc herniation,benefiting the kidney and passing the Governing Vessel is an important principle of treating lumbar disc herniation,and it can be carried through the whole process of treating lumbar disc herniation.

A mangiferin aglycon derivative J99745 has been identified as a potent xanthine oxidase (XOD) inhibitor by previous study. This study aimed to evaluate the hypouricemic effects of J99745 in experimental hyperuricemia mice, and explore the underlying mechanisms. Mice were orally administered 600 mg/kg xanthine once daily for 7 days and intraperitoneally injected 250 mg/kg oxonic acid on the 7th day to induce hyperuricemia. Meanwhile, J99745 (3, 10, and 30 mg/kg), allopurinol (20 mg/kg) or benzbromarone (20 mg/kg) were orally administered to mice for 7 days. On the 7th day, uric acid and creatinine in serum and urine, blood urea nitrogen (BUN), malondialdehyde (MDA) content and XOD activities in serum and liver were determined. Morphological changes in kidney were observed using hematoxylin and eosin (H&E) staining. Hepatic XOD, renal urate transporter 1 (URAT1), glucose transporter type 9 (GLUT9), organic anion transporter 1 (OAT1) and ATP-binding cassette transporter G2 (ABCG2) were detected by Western blot and real time polymerase chain reaction (PCR). The results showed that J99745 at doses of 10 and 30 mg/kg significantly reduced serum urate, and enhanced fractional excretion of uric acid (FEUA). H&E staining confirmed that J99745 provided greater nephroprotective effects than allopurinol and benzbromarone. Moreover, serum and hepatic XOD activities and renal URAT1 expression declined in J99745-treated hyperuricemia mice. In consistence with the ability to inhibit XOD, J99745 lowered serum MDA content in hyperuricemia mice. Our results suggest that J99745 exerts urate-lowering effect by inhibiting XOD activity and URAT1 expression, thus representing a promising candidate as an anti-hyperuricemia agent.