Objective： To observe the effect of Compound Shenhua Tablet （复方肾华片, SHT） on the sodium- potassium-exchanging adenosinetriphosphatase （Na＋-K＋-ATPase） in the renal tubular epithelial cells of rats with acute ischemic reperfusion and to investigate the mechanisms underlying the effects of SHT on renal ischemic reperfusion injury （RIRI）. Methods： Fifty male Wistar rats were randomly divided into the sham surgery group, model group, astragaloside group [150 mg/（kg.d）], SHT low-dose group [1.5 g/（kg,d）] and SHT high-dose group [3.0 g/（kg.d）], with 10 rats in each group. After 1 week of continuous intragastric drug administration, surgery was performed to establish the model. At either 24 or 72 h after the surgery, 5 rats in each group were sacrificed, blood biochemistry, renal pathology, immunoblot and immunohistochemical examinations were performed, and double immunofluorescence staining was observed under a laser confocal microscope. Results： Compared with the sham surgery group, the serum creatinine （SCr） and blood urea nitrogen （BUN） levels were significantly increased, Na＋-K＋-ATPase protein level was decreased, and kidney injury molecule-1 （KIM-1） protein level was increased in the model group after the surgery （P〈0.01 or P〈0.05）. Compared with the model group, the SCr, BUN, pathological scores, Na＋-K＋-ATPase, and the KIM-1 protein level of the three treatment groups were significantly improved at 72 h after the surgery （P〈0.05 or P〈0.01）. And the SCr, BUN of the SHT low- and high-dose groups, and the pathological scores of the SHT high-dose group were significantly lower than those of the astragaloside group （P〈0.05）. The Iocalizations of Na＋-K＋-ATPase and megalin of the model group were disrupted, with the distribution areas overlapping with each other and alternately arranged. The severity of the disruption was slightly milder in three treatment groups compared with that of the model group. The results of immunofluorescenc
Objective： TO study the prevention effect of salidroside on contrast-induced-nephropathy （CIN） and its underlying mechanism. Methods： A total of 24 Wistar rats were randomly divided into 4 groups with 6 in each group. Rats were firstly administrated with normal saline （control and model groups）, N-acetylcysteine （NAC, NAC group） and salidroside （salidroside group） for 7 days before model establishment in each group, respectively. Histopathological analysis was performed by periodic acid-Schiff （PAS） staining. Oxidative stress related parameters including superoxide dismutase （SOD） and methane dicarboxylic aldehyde （MDA）, nitric oxide （NO）, angiotensin 11 （Ang II）, 8-hydroxy-2＇-deoxyguanosine （8-OHdG）, mRNA and protein levels of endothelial nitric oxide synthase （eNOS）, and nitric oxide synthase （NOS） activity were measured. Results： Compared with the control group, the levels of MDA, Ang II and 8-OHdG were all significantly increased and levels of SOD, NO, and eNOS mRNA and protein were decreased significantly in the model group （P〈0.05）. Meanwhile, the NOS activity was also significantly decreased in the model group （P〈0.05）. In addition, the levels of these parameters were all improved in the NAC （P〈0.05） and salidroside groups and no significant different was found between these two groups （P〉0.05）. Conclusion： Salidroside can be the potential substitute Of NAC to prevent CIN. The underlying mechanism may be associated with oxidative stress damage caused by contrast agents.
Author＇s reply We read with great interest the letter of Yiginer, et al.regarding the influence of atrial fibrillation （AF） in the development of cognitive impairment in heart failure （HF） patients. The comment is related to the review published in the Journal by Leto, et al. that was a systematic overview about cognition, pathophysiology of cognitive impairment in heart failure patients. In the letter, Yiginer, et al.
Objective： To investigate the impact of a traditional Chinese medicinal compound known as Fufang Shenhua Tablet （复方肾华片, SHP） on the expression of Toll-like receptors （TLRs） during renal ischemia-reperfusion injury （IRI）-induced acute kidney injury （AKI） in rats. Methods： A total of 28 Wistar rats were randomly divided into five groups： （1） pseudo-operation control group, （2） ischemia-reperfusion model group, （3） Astragaloside group, （4） high-dose SHP group, and （5） low-dose SHP group. There were four rats in the pseudo-operation group and six rats in each of the other groups. The accepted ischemia-reperfusion model was established after a 7-day gavage intervention, and pathological changes and renal function were observed, using an enzyme-linked immunosorbent assay （ELISA） to detect interleukin 8 （IL-8） and interferon gamma （IFN-r） levels, as well as immunohistochemical staining to detect altered levels of TLR2 and TLR4 expression in renal tissue. Results： After 24 h, renal pathological damage and the expression levels of serum creatinine （Scr）, IL-8, IFN- r, TLR2, and TLR4 were significantly higher in the model group as compared with the pseudo-operation group （P〈0.05）. In addition, at 24 h the above indicators decreased significantly in the Astragaloside group, high- dose SHP group and low-dose SHP group as compared with the ischemia-reperfusion model group （P〈0.05）. TLR2 and TLR4 expression levels were significantly reduced in the SHP treatment and Astragaloside group as compared with the pseudo-operation group （P〈0.05）. Further, the high-dose SHP group showed significantly less renal damage score and decreased levels of TLR expression than those of low-dose SHP group and Astragaloside group （all P〈0.05）. Conclusion： SHP can alleviate the renal structural and functional damage caused by IRI-induced AKI in rats by reducing the damage of renal pathology, which may reduce inflammatory cytokine levels by downregulating
