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Objective: To compare the effect of short-term calorie restriction (CR) on aging with that of already known long-term CR, the anti-inflammatory efficacy of 10-day CR was explored in aged rat kidney., Treatment: Two different age groups, 6 months (young) and 24 months (old) were used. In the old group, one sub-group was control, fed ad libitum (AL) and the other was fed CR for 10 days with 40 % of the food intake of the AL subgroup (n = 5)., Methods: Reactive species (RS), lipid peroxides and COX-2 activity were measured. The activities of proinflammatory transcription factors NF-kB and AP-1 were measured by electro-mobility shift assay (EMSA). Upstream signaling cascades of NF-kB and AP-1 as well as proinflammatory gene expression were detected by Western blot., Results: 10-day CR suppressed RS, lipid peroxides, and COX-2 activity in aged rat kidney. CR also inhibited upstream signaling cascades and DNA binding activity of NF-kB and AP-1, and thioredoxin/Ref-1 pathway. CR blocked expression of NF-kB-and AP-1-responsive gene COX-2, iNOS, VCAM-1 and ICAM-1., Conclusions: We report for the first time that 10-day CR can attenuate the altered signaling transduction for inflammatory processes which is mediated through RS-induced NF-kB and AP-1 in aged kidney.

Renal carcinoid tumours are uncommon. The aetiology is not yet fully understood and there is still no useful diagnostic tool for detecting them. We report our experience managing a Chinese woman with a primary renal carcinoid tumour.

Xanthine oxidoreductase (XD: xanthine dehydrogenase + xanthine oxidase) is a complex enzyme that catalyzes oxidation of hypoxathine to xanthine, subsequently producing uric acid. The enzyme complex exists in separate but interconvertible forms, xanthine dehydrogenase (XDH) and xanthine oxidase (XOD). XOD is one of the major cellular sources of superoxide production and is well known as a causative factor in ischemia/reperfusion damage. At present, almost no information on the conversion status is available with respect to aging. In the present study, we investigated the effect of age on the XOD/XDH status and gene expression in the kidney. In addition, we assessed XOD-induced reactive oxygen species (ROS) using the dichlorofluoroscein (DCF) method. Our results show that XD activity gradually up to 18 months of age and then a slight decrease at 24 months of age. XDH activity showed increases up to 18 months of age, then decreased at 24 months of age. The conversion of XDH to XOD, assessed by changes in the ratios of XOD/(XOD+XDH), showed an age-related increase, which peaked at 24 months. Levels of XD protein and its mRNA paralleled to overall XD activity. ROS generation has tendency to increase with age. Our results suggest that the increased conversion of XDH to XOD observed with age may be an important contributing factor to the increased renal oxidative stress during aging.

The effect of magnesium lithospermate B purified from Salviae Miltiorrhizae Radix on the kinin-prostaglandin E2 system was investigated using kidney slices and isolated kidney microsomes. Magnesium lithospermate B markedly increased the amount of thiobarbituric acid-reactive substances produced by incubation of arachidonic acid in renal slices. Enhancement of arachidonic acid-mediated oxygenation of 1,3-diphenylisobenzofuran was also observed in renal microsomes from rats treated with magnesium lithospermate B, indicating an increase of prostaglandin biosynthesis. Furthermore, magnesium lithospermate B significantly increased the synthesis of prostaglandin E2 in renal slices, but the magnesium lithospermate B-mediated response was blunted with kinin antagonist. On the basis of the above results, it is apparent that magnesium lithospermate B exerts an influence on the prostaglandin system via kinin receptors.

Renal responses to magnesium lithospermate B isolated from Salviae miltiorrhizae radix were examined in normal rats. Urinary sodium, potassium, prostaglandin E2 and kallikrein excretion was significantly increased after magnesium lithospermate B administration, whereas excretion of urinary 6-keto-prostaglandin F1 alpha and thromboxane B2 was unchanged. Rats administered with the drug also revealed a slight elevation of plasma renin activity and the levels of angiotensins I and II. Plasma aldosterone was decreased slightly. No significant changes were observed in angiotensin-converting enzyme or blood pressure.

The effect of magnesium lithospermate B on the renal responses of rats with renal failure was investigated in the presence and absence of pretreatment with the kallikrein inhibitor, aprotinin. Magnesium lithospermate B caused a marked increase in the levels of the renal functional parameters (glomerular filtration rate, renal plasma flow and renal blood flow), accompanied by significant increases in urinary prostaglandin excretion (increases of prostaglandin E2 and 6-keto-prostaglandin F1 alpha excretion by 82% and 36%, respectively). The urinary excretion of kallikrein was also increased following magnesium lithospermate B administration. However, pretreatment with aprotinin abolished the renal function-facilitating action of magnesium lithospermate B concomitantly with a markedly increased urinary excretion of prostaglandin E2, 6-keto-prostaglandin F1 alpha and kallikrein. These results suggest that the kallikrein-kinin-prostaglandin B.

The glomerular filtration rate (GFR), renal plasma flow (RPF) and renal blood flow (RBF) were all markedly decreased in rats given an adenine diet as the period of adenine administration lengthened. Concurrently, the urinary excretions of prostaglandin E2 (PGE2) and 6-keto-prostaglandin F1 alpha(6-keto-PGF1 alpha) decreased gradually in parallel with the renal function parameters, whereas the urinary excretion of thromboxane B2 (TXB2) increased markedly. These findings suggest the involvement of prostaglandin in the renal circulation.

The involvement of prostanoids in the improvement of adenine-induced renal failure in rats by magnesium lithospermate B was studied. After intraperitoneal administration of magnesium lithospermate B to renal failure rats, the levels of glomerular filtration rate, renal plasma flow and renal blood flow were increased. Urinary excretions of prostaglandin E2 (PGE2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) in renal failure rats were increased by the administration of magnesium lithospermate B, while that of thromboxane B2 had no effect. Pretreatment with indomethacin abolished the improving effect of magnesium lithospermate B on renal function concomitantly with markedly suppressed urinary excretion of prostanoids. These results suggest that the increased formation of PGE2 and 6-keto-PGF1 alpha might contribute to the improvement of adenine-induced renal failure in rats by magnesium lithospermate B.