Abstract
Objectives. Hyperuricemia (HUA) is a disease caused by increased production of uric acid (UA) or reduced excretion of UA in the body. Results of an epidemiological survey show that 60% of patients with HUA have hyperlipidemia (HPA). Dendrobium officinalis (DOF) six nostrum (DOS) is based on the theory of traditional Chinese medicine for the transformation of the traditional Chinese nostrum Si Miao Wan. In this article, we aim to discuss the efficacy and mechanism of DOS in reducing UA and regulating lipid metabolism. The rat model of HUA with HPA was induced by potassium oxonate (PO) combined with high-fat sorghum feed. We monitored the serum UA and blood lipids. Liver xanthine oxidase (XOD), adenosine deaminase (ADA), lipoprotein lipase (LPL), and fatty acid-binding protein (FABP1) activities were measured by enzyme-linked immunosorbent assay (ELISA) after the last administration of DOS. We performed a histopathological examination of rat kidney and intestine. Immunohistochemistry (IHC) was used to detect the expression of renal inflammatory proteins NLRP3 / Caspase-1 and intestinal inflammatory proteins TLR4 / NLRP3. We used western blot for measurement of liver hypoxanthine-guanine phosphoribosyl transferase (HPRT1) protein expression and renal PDZ domain protein kidney 1 (PDZK1) protein expression. DOS administration significantly reduced serum UA, total cholesterol (TC), and low-density lipoprotein cholesterol (LDL-c) level, and improved liver steatosis in the model rat. At the same time, DOS treatment effectively inhibited liver XOD and ADA, increased the level of liver HPRT1, and reduced the production of UA. Additional studies had shown that DOS can restore normal UA excretion function in the intestine and kidney and regulated liver lipids metabolism. IHC and histopathological sections showed that DOS reduced the level of kidney, intestinal inflammatory body (NLRP3, Caspase-1, and TLR4), improved inflammation of the kidney and intestinal tract in rats. DOS is a promising drug that can effectively reduce serum UA and lipid level in the model rat. The mechanism of action may be related to inhibition of UA production, promotion of UA excretion, regulation of lipids metabolism, and anti-inflammatory response.
Highlights
Hyperuricemia (HUA) is often caused by hereditary and acquired causes of decreased uric acid (UA) excretion or increased UA production
It can be hypothesized that abnormal UA metabolism and abnormal serum lipid metabolism interact in the body to form a vicious circle, which leads to aggravation in patients with HUA and HPA
As shown in Figures 1(a)∼1(c), after modeling for 4 weeks, compared with the normal control (NC) group, the serum uric acid (SUA) level of rats in each model control (MC) group increased significantly (P < 0.01, P < 0.05), suggesting that the SUA level of rats fed with high-fat sorghum feed for 4 weeks could significantly increase
Summary
Hyperuricemia (HUA) is often caused by hereditary and (or) acquired causes of decreased uric acid (UA) excretion or increased UA production. Both of these scenarios cause UA to accumulate in the body, resulting in a continuous increase in blood UA [1]. Elevated serum uric acid (SUA) aggravates lipid metabolism disorders and increases the risk of high lowdensity lipoprotein cholesterol (LDL-c) [5], while abnormal lipid metabolism can aggravate SUA level [6]. It can be hypothesized that abnormal UA metabolism and abnormal serum lipid metabolism interact in the body to form a vicious circle, which leads to aggravation in patients with HUA and HPA
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