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The potential mechanism of INHBC and CSF1R in diabetic nephropathy
1Department of Nephrology, Jining No. 1 People's Hospital, Jining, P.R. China. zhoushiju@sina.com.
Objective:
The aim of this study was to research the potential mechanism of INHBC and CSF1R in diabetic nephropathy.
Materials And Methods:
30 SD rats were selected and randomly divided into Con group, Sham group, and DN group. In the DN group, intraperitoneal injection of the streptozotocin-citrate solution was conducted to construct the DN model. In the Sham group, intraperitoneal injection of equal citrate solution was conducted. The Con group did not do anything. After successful modeling, blood glucose, insulin, biochemical indexes, and levels of inflammatory cytokines in blood samples were detected. The expression levels of INHBC, CSF1R, apoptosis-related proteins and IGF-1 were detected by Western blot. MRNA expression levels of INHBC, CSF1R, IGF-1 and inflammatory cytokines were detected by qPCR.
Results:
Compared with the Con group, the expression levels of blood glucose, insulin, biochemical indexes, INHBC, CSF1R, IGF-1, IL-6, TNF-α and Bcl2 increased in the DN group, while the expression levels of IL-10, Caspase 3, Caspase 9, and Bax decreased. INHBC mRNA was positively correlated with IGF-1 mRNA. CSF1R was negatively correlated with Caspase 3, Caspase 9, Bax, and IL-10, and positively correlated with IL-6, TNF-α, and Bcl2.
Conclusions:
NHBC and CSF1R induced the secretion of IL-6 and TNF-α, inhibited the production of IL-10, inhibited apoptosis of cells, and promoted the proliferation of renal cells during DN disease. Therefore, INHBC and CSF1R can be used as target objects of DN treatment strategies.
Insights
In diabetic nephropathy (DN), Inhibin beta C (INHBC) and Colony-stimulating factor 1 receptor (CSF1R) promote inflammation and inhibit apoptosis. Targeting INHBC and CSF1R may offer new therapeutic strategies for DN.
Area of Science:
- Nephrology
- Endocrinology
- Molecular Biology
Background:
- Diabetic nephropathy (DN) is a major complication of diabetes mellitus.
- Understanding the molecular mechanisms underlying DN is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the potential roles and mechanisms of Inhibin beta C (INHBC) and Colony-stimulating factor 1 receptor (CSF1R) in diabetic nephropathy.
- To explore INHBC and CSF1R as potential therapeutic targets for DN.
Main Methods:
- A diabetic nephropathy rat model was established using streptozotocin.
- Blood glucose, insulin, biochemical markers, and inflammatory cytokines were analyzed.
- Expression levels of INHBC, CSF1R, apoptosis-related proteins, and IGF-1 were assessed using Western blot and qPCR.
Main Results:
- Diabetic nephropathy rats exhibited increased blood glucose, insulin, INHBC, CSF1R, IGF-1, IL-6, TNF-α, and Bcl2.
- Levels of IL-10, Caspase 3, Caspase 9, and Bax were decreased in DN rats.
- INHBC mRNA correlated positively with IGF-1 mRNA; CSF1R expression correlated with inflammatory and apoptotic markers.
Conclusions:
- INHBC and CSF1R contribute to DN by inducing pro-inflammatory cytokines (IL-6, TNF-α), inhibiting anti-inflammatory cytokine (IL-10), suppressing apoptosis, and promoting renal cell proliferation.
- INHBC and CSF1R represent promising therapeutic targets for managing diabetic nephropathy.
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