The mechanism of blood concentrations of the Shenqi pill repairing injured epithelial cells of renal tubular in vitro
- Authors:
View Affiliations
Affiliations: Department of Nephrology, The Central Hospital of Enshi Tujia and Miao Autonomous Prefecture, Enshi, Hubei 445000, P.R. China, Department of Pharmacy, The Central Hospital of Enshi Tujia and Miao Autonomous Prefecture, Enshi, Hubei 445000, P.R. China
- Published online on: May 11, 2017 https://doi.org/10.3892/etm.2017.4450
-
Pages:
246-250
-
Copyright: © Huang
et al. This is an open access article distributed under the
terms of Creative
Commons Attribution License.
Metrics: Total
Views: 0 (Spandidos Publications: | PMC Statistics: )
Metrics: Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
This article is mentioned in:
Abstract
In the present study, we investigated the best blood concentration of the mechanism of Shenqi pill repairing the injured epithelial cells of renal tubular in vitro. First, the injured hypoxia/reoxygenation model of rat proximal renal tubular epithelial cell strain (NRK-52E) was established. The animals were divided randomly into control, model, low concentration (5 µg/ml), moderate concentration (10 µg/ml) and high concentration (20 µg/ml) groups. The apoptotic rate was measured with flow cytometry and Jag2/Notch2/hes1 mRNA, and the protein expression was measured for 1, 3 and 7 days. It was found that in comparison to the control group, the growth of each group was prolonged with time, the levels of apoptosis, and the Jag2/Notch2/hes1 mRNA and protein expression decreased. Furthermore, the levels of the apoptotic rate, Jag2/Notch2/hes1 mRNA and protein expression of the moderate concentration and high concentration groups were significantly lower than those of the model and low‑dose groups at each time‑point (P<0.05). In conclusion, the Shenqi Pill alleviates the damage of renal tubular epithelial cells by inhibiting the Jag2/Notch2/hes1 signaling pathway; suitable concentration such as 10-20 µg/ml can exert protective effect.
View References
|
1
|
Gao Y, Zeng Z, Li T, Xu S, Wang X, Chen Z
and Lin C: Polydatin inhibits mitochondrial dysfunction in the
renal tubular epithelial cells of a rat model of sepsis-induced
acute kidney injury. Anesth Analg. 121:1251–1260. 2015. View Article : Google Scholar : PubMed/NCBI
|
|
2
|
Li K, Han Q, Yan X, Liao L and Zhao RC:
Not a process of simple vicariousness, the differentiation of human
adipose-derived mesenchymal stem cells to renal tubular epithelial
cells plays an important role in acute kidney injury repairing.
Stem Cells Dev. 19:1267–1275. 2010. View Article : Google Scholar : PubMed/NCBI
|
|
3
|
Cheng HT and Kopan R: The role of Notch
signaling in specification of podocyte and proximal tubules within
the developing mouse kidney. Kidney Int. 68:1951–1952. 2005.
View Article : Google Scholar : PubMed/NCBI
|
|
4
|
Huang R, Zhou Q, Veeraragoo P, Yu H and
Xiao Z: Notch2/Hes-1 pathway plays an important role in renal
ischemia and reperfusion injury-associated inflammation and
apoptosis and the γ-secretase inhibitor DAPT has a nephroprotective
effect. Ren Fail. 33:207–216. 2011. View Article : Google Scholar : PubMed/NCBI
|
|
5
|
Nan Y, Zhou X, Liu Q, Zhang A, Guan Y, Lin
S, Kong L, Han Y and Wang X: Serum metabolomics strategy for
understanding pharmacological effects of ShenQi pill acting on
kidney yang deficiency syndrome. J Chromatogr B Analyt Technol
Biomed Life Sci. 19:102–103. 2015.
|
|
6
|
Xiong X, Wang P, Li X and Zhang Y: Shenqi
pill, a traditional Chinese herbal formula, for the treatment of
hypertension: a systematic review. Complement Ther Med. 23:484–493.
2015. View Article : Google Scholar : PubMed/NCBI
|
|
7
|
Kramer J, Schwanbeck R, Pagel H, Cakiroglu
F, Rohwedel J and Just U: Inhibition of Notch signaling ameliorates
acute kidney failure and downregulates platelet-derived growth
factor receptor β in the mouse model. Cells Tissues Organs.
201:109–117. 2016. View Article : Google Scholar : PubMed/NCBI
|
|
8
|
Juillerat-Jeanneret L, Flohr A, Schneider
M, Walter I, Wyss JC, Kumar R, Golshayan D and Aebi JD: Targeted
γ-secretase inhibition to control the Notch pathway in renal
diseases. J Med Chem. 58:8097–8109. 2015. View Article : Google Scholar : PubMed/NCBI
|
|
9
|
Long YL and Li ZM: Effect of jingui shenqi
pill and its disassembled recipes on ovarian functions in shen yang
deficiency female rats. Zhongguo Zhong Xi Yi Jie He Za Zhi.
33:967–971. 2013.(In Chinese). PubMed/NCBI
|
|
10
|
Xu CP, Zhu QJ, Song J, Li Z and Zhang D:
Acceleration of Jingui Shenqi Pill on the testis telomerase
activity in mice of Shen-yang deficiency. Zhongguo Zhong Xi Yi Jie
He Za Zhi. 33:252–255. 2013.(In Chinese). PubMed/NCBI
|
|
11
|
Sörensen-Zender I, Rong S, Susnik N,
Zender S, Pennekamp P, Melk A, Haller H and Schmitt R: Renal
tubular Notch signaling triggers a prosenescent state after acute
kidney injury. Am J Physiol Renal Physiol. 306:F907–F915. 2014.
View Article : Google Scholar : PubMed/NCBI
|
