This article contains findings obtained from research on animals:
- The results from animal research studies should not be directly applied to humans and the results may not generalise to the human population.
- There may be significant differences between species in terms of physiology, physiology, and pharmacology, as well as differences in the way diseases and treatments are modelled in animals.
- Any conclusions drawn from animal research should be considered with caution and in the context of other types of research studies such as observational studies, clinical trials, and reviews of the literature.
Insights & Discussion
The Jian-Pi-Yi-Shen (JPYS) traditional Chinese medicine formula aids in the alleviation of renal dysfunction and fibrosis in chronic kidney disease (CKD) rats by combating inflammation and cellular apoptosis.
Using an established model of 5/6 nephrectomized (5/6Nx) rats, an evaluation of the effects of the JPYS formula on renal function and fibrosis was conducted. To scrutinize the formula's impacts, markers of apoptosis, inflammation, oxidative stress, and the activity of Nrf2 signaling were measured. Correlative parameters including urinary protein, SCr, BUN, glomerular sclerosis index, tubulointerstitial fibrosis score, and renal histopathology were analyzed to assess the formula's preventive effect on renal dysfunction and fibrosis. The study also evaluated the gene expression associated with fibrosis and related elements such as TGF-β and various types of collagen.
The evaluation of JPYS's efficacy revealed significant protection against cell apoptosis, highlighted by altered gene expression of Bcl-2, Bax, caspase 3, caspase 9, and the number of TUNEL-positive cells. Moreover, it was observed that the JPYS formula countered the activation of the NF-κB-mediated inflammatory pathway, exhibiting a decrease in gene expression of numerous inflammatory markers in the kidney. Alongside this, the formula promoted antioxidant performance, alleviating oxidative stress as indicated by antioxidant index indicators and a reduction in reactive oxygen species biomarkers. The study also identified the upswing of essential elements like HO-1 and Nrf2 level and a decline in Keap1 expression, signaling rationale towards the formula's potential relief of renal oxidative damage.
Discover Related Insights
The herbal decoction Jian-Pi-Yi-Shen reduces symptoms of chronic kidney disease and anaemia by improving iron metabolism and inhibiting the JAK2-STAT3 signaling pathway.
2023 Journal of Ethnopharmacology Jian-Pi-Yi-Shen formula restores iron metabolism from dysregulation in anemic rats with adenine-induced nephropathy Li C, Huang H, Wang R, Zhang C, Huang S, Wu J, et al.
Experimental Study Anaemia Chronic Kidney Disease Jian Pi Yi Shen Formula
Methodology used included an analysis of network pharmacology, chemical profiling, and in vivo experiments on the effect of Jian-Pi-Yi-Shen (JPYS) on renal anemia and chronic kidney disease (CKD). The active compounds in JPYS were detected in in vivo experiment, and their potential targets were predicted by network pharmacology. An animal model of CKD-related anemia was developed using adenine-feeding for further analysis. The estimation of renal injury was conducted using blood tests, histopathological examinations, and fibrosis degree assessment while the levels of JAK2, STAT3 and iron metabolism-related factors were measured through various techniques.
Discussion of the results reveals that 164 active ingredients, including prototypes and metabolites in JPYS, were discovered and 21 core targets were identified. Many of these core targets were associated with the JAK2-STAT3 signaling pathways. Experimental results demonstrated that JPYS treatment significantly improved hematological parameters and iron metabolism in CKD rats, decreased certain indicators of renal damage, and suppressed the expression of JAK2 and STAT3.
Jian-Pi-Yi-Shen formula has shown potential in delaying kidney deterioration in chronic kidney disease by rejuvenating the process of creating nicotinamide adenine dinucleotide.
2023 Aging Jian-Pi-Yi-Shen formula alleviates renal fibrosis by restoring NAD+ biosynthesis in vivo and in vitro Gao L, Huang X, Deng R, Wu S, Peng Y, Xiong G, et al.
Experimental Study Chronic Kidney Disease Jian Pi Yi Shen Formula Renal Fibrosis
The study was conducted utilizing an adenine-diet feeding model for inducing chronic kidney disease in a breed of mice. For 4 weeks, these mice were given Jian-Pi-Yi-Shen formula orally. Human proximal tubular epithelial cells were stimulated with a growth factor, with or without the formula. Assessments were made of renal function via serum creatinine and blood urea nitrogen levels, with renal histopathological changes evaluated through specific staining techniques. Further, cell viability and NAD+ concentrations were monitored with assay kits.
The Jian-Pi-Yi-Shen formula did not only help in the improvement of renal function and reduction of pathological injury but it also inhibited renal fibrosis in the mice with chronic kidney disease. Moreover, the same formula was found to reverse fibrotic responses induced by a growth factor in human proximal tubular epithelial cells. Importantly, the formula was observed to recover the decreased NAD+ content in the chronic kidney disease mice and the human cells, bringing about the restoration of the expression of vital enzymes in the NAD+ synthesis process.
Jian-Pi-Yi-Shen, a traditional Chinese medicine, helps treat anemia in chronic kidney disease by stimulating erythropoietin production and regulating iron recycling.
2020 Evidence-Based Complementary and Alternative Medicine Jian-Pi-Yi-Shen Regulates EPO and Iron Recycling Protein Expressions in Anemic Rats with Chronic Kidney Disease: Accumulation of Hypoxia Inducible Factor-2α via ERK Signaling Wang F, Yu H, Huang S, Zheng L, Zheng P, Zhang S, et al.
Animal Study Anaemia Chronic Kidney Disease Erythropoietin
To investigate the effect of Jian-Pi-Yi-Shen (JPYS), chronic kidney disease (CKD) was experimentally induced in rats using a 5/6 nephrectomy. The rats were then administered JPYS orally in both high and low doses for a period of 90 days. Observations were made regarding the serum hepcidin level to assess iron homeostasis. Additionally, the protein expressions of hypoxia inducible factor-2, erythropoietin, ferritin, ferroportin, and the phosphorylation level of extracellular signal-regulated kinase 1/2 were studied using Western blot analysis.
The results showed that JPYS treatment significantly improved kidney function in the CKD rats. Alongside this, pathological kidney damage was found to be significantly restored post-JPYS treatment. The medicine was found to be effective in improving anemia in CKD through the upregulation of red blood cells, hemoglobin, and hematocrit levels. It was also discovered that JPYS stimulates the expressions of erythropoietin and hypoxia-inducible factor-2 proteins in the kidney and liver of the CKD rats, while inducing the phosphorylation of extracellular signal-regulated kinase 1/2 proteins. Furthermore, JPYS was seen to regulate the protein expressions of ferritin and ferroportin in the liver and spleen, as well as in the serum level of hepcidin, suggesting its role in systemic iron recycling.
The Jian-Pi-Yi-Shen formula appears to slow down chronic kidney disease progression by inhibiting inflammation via the nuclear factor-kappa B signaling pathway.
2018 Evidence-Based Complementary and Alternative Medicine Jian‐Pi‐Yi‐Shen Formula Regulates Inflammatory Cytokines Production in 5/6 Nephrectomized Rats via Suppression of NF‐κB Activation Lu J, Liu X, Liao Y, Wang D, Chen J, Li S
Experimental Study Chronic Kidney Disease Jian Pi Yi Shen Formula
In the method used for this study, a rat model was established using a 5/6 nephrectomy process. The rats were then segregated into two groups: one group given the Jian-Pi-Yi-Shen formula treatment, and another group that served as a control. The formula, measured at a dosage of 2.06g/kg per day, was administered to the rats via gavage over a six-week period.
The results from this study revealed that the Jian-Pi-Yi-Shen formula treatment led to a substantial improvement in kidney function and a reduction in pathological injury in the rat model. A Multiplex analysis of various cytokines indicated that the formula triggered a reduction in proinflammatory cytokines and an increase in anti-inflammatory cytokine production. Additionally, the formula was found to inhibit the activation of the nuclear factor-kappa B signaling pathway that is typically associated with inflammation.
The Jian-Pi-Yi-Shen Formula (JPYSF) has been found to significantly improve chronic kidney disease, potentially through the modulation of the mitochondrial quality control network.
2018 BMC Complementary Medicine and Therapies Jian-Pi-Yi-Shen Formula ameliorates chronic kidney disease: involvement of mitochondrial quality control network Liu X, Chen J, Liu X, Wang D, Zheng P, Qi A, et al.
Experimental Study Chronic Kidney Disease Jian Pi Yi Shen Formula
In the study, 5/6 nephrectomized rats were treated daily for six weeks with the Chinese herbal concoction Jian-Pi-Yi-Shen Formula and Perindopril administered orally. Signs of chronic kidney disease were studied, such as renal function, pathological harm, and fibrosis, and were evaluated. Protein levels connected to the mitochondrial quality control network were measured using Western blot and immunofluorescence analysis techniques.
The research observed that the rats presented significantly decreased kidney function and qualitative injuries in kidney structure, evidenced by increased blood urea nitrogen, serum creatinine, urinary protein excretion, and signs of glomerular hypertrophy, tubular atrophy, and interstitial fibrosis. By administering the JPYSF, both the kidney function and structure saw an improvement. Further analysis unveiled that the residual kidneys of the rats had an unbalanced mitochondrial quality control network characterized by decreased mitochondrial fusion, biogenesis, mitophagy, and increased mitochondrial fission. This imbalance was rectified through treatment with the JPYSF, thus suggesting a potential therapeutic pathway.
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