Abstract
Xianling Gubao Capsule (XGC), a kind of capsule preparation of Chinese herbal officially approved for sale by the National Medical Products Administration (NMPA), has the effect of tonifying kidney and strengthening bones. Although the impact of XGC in treating bone diseases has been widely studied, the effect of XGC in kidney injury is unknown yet. The kidney injury model is established by intraperitoneal injection with cadmium chloride (CdCl2). Before model establishment, each XGC group was pregavaged with XGC for 10 d. After 10 d, CdCl2 was injected intraperitoneally into the model group and each XGC group, each XGC group continued to be gavaged with XGC for 4 weeks, and the control group was gavaged with equal doses of distilled water once daily. The level of serum urea nitrogen (BUN) and serum creatinine (Cr) is evaluated by kit. The effect of XGC on protecting kidney injury in mice with kidney injury is analyzed by histopathology (HE stain), immunohistochemistry (IHC), and real-time fluorescence quantitative PCR (RT-qPCR). The results show that CdCl2 significantly increases the level BUN and Cr in serum and results in remarkable pathological changes in the nephron, including tubule edema, congestion, and necrosis. While oral administration of XGC can significantly decrease BUN and Cr in serum and prevent and protect the kidney from the above injuries. In addition, the protein expression of p-mTOR was remarkably reduced, and the ratio of LC3II/LC3I protein and mRNA was significantly increased in mice with oral administration of XGC. Our findings suggest that XGC can prevent and protect kidney injury by improving the state of renal tubular hyperemia and necrosis and reduce the level of BUN and Cr in cadmium poisoning mice.
Highlights
Kidney injury is a global public health problem, causing 1.7 million deaths each year
If the patient cannot recover from the kidney injury, it will develop into chronic kidney disease (CKD) and eventually develop into renal failure [2]
When acute kidney injury (AKI) occurs, autophagy is activated in renal tubular epithelial cells, and blocking autophagy will lead to the deterioration of the disease, while inducing autophagy can reduce the injury [5, 6]
Summary
Kidney injury is a global public health problem, causing 1.7 million deaths each year. Many reasons can cause kidney injury, such as sepsis, drugs, and toxins. There are usually tubulointerstitial and glomerular lesions in the tissue [1]. If the patient cannot recover from the kidney injury, it will develop into chronic kidney disease (CKD) and eventually develop into renal failure [2]. The final death caused by chronic renal injury has caused a severe social crisis, so people have carried out a lot of research in this field. When acute kidney injury (AKI) occurs, autophagy is activated in renal tubular epithelial cells, and blocking autophagy will lead to the deterioration of the disease, while inducing autophagy can reduce the injury [5, 6]. It is essential to prevent the treatment of diseases other than kidney injury
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