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[Effects and mechanisms of huangkui capsule ameliorating renal fibrosis in diabetic nephropathy rats via inhibiting oxidative stress and p38MAPK signaling pathway activity in kidney].
Zhongguo Zhong Yao Za Zhi. 2014 Nov; 39(21):4110-7.ZZ

Abstract

OBJECTIVE

To demonstrate the effects and mechanisms of Huangkui capsule (HKC) on renal fibrosis in rats with diabetic nephropathy (DN).

METHOD

Rats were randomly divided into 5 groups, the sham-operated group (Sham group, n = 5), the vehicle-given group (Vehicle group, n = 7), the low dose of HKC-treated group (L-HKC group, n = 7), the high dose of HKC-treated group (H-HKC group, n = 7) and the lipoic acid (LA)-treated group (LA group, n = 7). DN models were induced by intraperitoneal injection of streptozotocin (STZ,35 mg x kg(-1)) twice and unilateral nephrectomy. After models were successfully established, the rats in HKC and LA groups were daily administrated with HKC suspensions (0.75, 2 g x kg(-1)) or LA suspensions (60 mg x kg(-1)) respectively, and at the same time, the rats in Vehicle group were daily administrated with distilled water (2 mL) for 8 weeks. All rats were sacrificed at the end of week 8 to collect blood and renal tissues. UAlb, renal function, renal fibrotic morphologic characteristics, as well as oxidative stress (OS)-related markers, the protein expressions of the key signaling molecules in p38 mitogen-activated protein kinase (p38MAPK) signaling pathway, fibrogenic cytokines and inflammatory factors were examined respectively.

RESULT

HKC, similar to LA, improved the general state of health, body weight, UAlb, BUN, UA and Alb in DN model rats. Of note, renal fibrosis was ameliorated in HKC groups,especially in H-HKC group which was better than that in LA group. In addition, HKC not only improved the main indexes of OS in the kidney like LA, but also down-regulated the protein expressions of phosphorylated-p38MAPK (p-p38MAPK), transforming growth factor (TGF)-β1 and tumor necrosis factor(TNF)-α in the kidney, whereas, LA only decreased the protein expression of TNF-α in the kidney in DN model rats.

CONCLUSION

HKC, similar to LA, has the actions of anti-OS in vivo. Moreover, HKC could attenuate renal fibrosis by suppressing the activation of p38MAPK signaling pathway and the protein expressions of fibrogenic cytokines and inflammatory factors in the kidney in DN model rats, which is different from LA.

Authors

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Pub Type(s)

English Abstract
Journal Article
Research Support, Non-U.S. Gov't

Language

chi

PubMed ID

25775777

Citation

Mao, Zhi-min, et al. "[Effects and Mechanisms of Huangkui Capsule Ameliorating Renal Fibrosis in Diabetic Nephropathy Rats Via Inhibiting Oxidative Stress and p38MAPK Signaling Pathway Activity in Kidney]." Zhongguo Zhong Yao Za Zhi = Zhongguo Zhongyao Zazhi = China Journal of Chinese Materia Medica, vol. 39, no. 21, 2014, pp. 4110-7.
Mao ZM, Wan YG, Sun W, et al. [Effects and mechanisms of huangkui capsule ameliorating renal fibrosis in diabetic nephropathy rats via inhibiting oxidative stress and p38MAPK signaling pathway activity in kidney]. Zhongguo Zhong Yao Za Zhi. 2014;39(21):4110-7.
Mao, Z. M., Wan, Y. G., Sun, W., Chen, H. L., Huang, Y. R., Shi, X. M., & Yao, J. (2014). [Effects and mechanisms of huangkui capsule ameliorating renal fibrosis in diabetic nephropathy rats via inhibiting oxidative stress and p38MAPK signaling pathway activity in kidney]. Zhongguo Zhong Yao Za Zhi = Zhongguo Zhongyao Zazhi = China Journal of Chinese Materia Medica, 39(21), 4110-7.
Mao ZM, et al. [Effects and Mechanisms of Huangkui Capsule Ameliorating Renal Fibrosis in Diabetic Nephropathy Rats Via Inhibiting Oxidative Stress and p38MAPK Signaling Pathway Activity in Kidney]. Zhongguo Zhong Yao Za Zhi. 2014;39(21):4110-7. PubMed PMID: 25775777.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Effects and mechanisms of huangkui capsule ameliorating renal fibrosis in diabetic nephropathy rats via inhibiting oxidative stress and p38MAPK signaling pathway activity in kidney]. AU - Mao,Zhi-min, AU - Wan,Yi-gang, AU - Sun,Wei, AU - Chen,Hao-li, AU - Huang,Yan-ru, AU - Shi,Xi-miao, AU - Yao,Jian, PY - 2015/3/18/entrez PY - 2015/3/18/pubmed PY - 2015/5/1/medline SP - 4110 EP - 7 JF - Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica JO - Zhongguo Zhong Yao Za Zhi VL - 39 IS - 21 N2 - OBJECTIVE: To demonstrate the effects and mechanisms of Huangkui capsule (HKC) on renal fibrosis in rats with diabetic nephropathy (DN). METHOD: Rats were randomly divided into 5 groups, the sham-operated group (Sham group, n = 5), the vehicle-given group (Vehicle group, n = 7), the low dose of HKC-treated group (L-HKC group, n = 7), the high dose of HKC-treated group (H-HKC group, n = 7) and the lipoic acid (LA)-treated group (LA group, n = 7). DN models were induced by intraperitoneal injection of streptozotocin (STZ,35 mg x kg(-1)) twice and unilateral nephrectomy. After models were successfully established, the rats in HKC and LA groups were daily administrated with HKC suspensions (0.75, 2 g x kg(-1)) or LA suspensions (60 mg x kg(-1)) respectively, and at the same time, the rats in Vehicle group were daily administrated with distilled water (2 mL) for 8 weeks. All rats were sacrificed at the end of week 8 to collect blood and renal tissues. UAlb, renal function, renal fibrotic morphologic characteristics, as well as oxidative stress (OS)-related markers, the protein expressions of the key signaling molecules in p38 mitogen-activated protein kinase (p38MAPK) signaling pathway, fibrogenic cytokines and inflammatory factors were examined respectively. RESULT: HKC, similar to LA, improved the general state of health, body weight, UAlb, BUN, UA and Alb in DN model rats. Of note, renal fibrosis was ameliorated in HKC groups,especially in H-HKC group which was better than that in LA group. In addition, HKC not only improved the main indexes of OS in the kidney like LA, but also down-regulated the protein expressions of phosphorylated-p38MAPK (p-p38MAPK), transforming growth factor (TGF)-β1 and tumor necrosis factor(TNF)-α in the kidney, whereas, LA only decreased the protein expression of TNF-α in the kidney in DN model rats. CONCLUSION: HKC, similar to LA, has the actions of anti-OS in vivo. Moreover, HKC could attenuate renal fibrosis by suppressing the activation of p38MAPK signaling pathway and the protein expressions of fibrogenic cytokines and inflammatory factors in the kidney in DN model rats, which is different from LA. SN - 1001-5302 UR - https://www.unboundmedicine.com/medline/citation/25775777/[Effects_and_mechanisms_of_huangkui_capsule_ameliorating_renal_fibrosis_in_diabetic_nephropathy_rats_via_inhibiting_oxidative_stress_and_p38MAPK_signaling_pathway_activity_in_kidney]_ L2 - https://medlineplus.gov/diabetickidneyproblems.html DB - PRIME DP - Unbound Medicine ER -