Baicalin inhibits the expression of monocyte chemoattractant protein-1 and interleukin-6 in the kidneys of apolipoprotein E-knockout mice fed a high cholesterol diet

Abstract

Hyperlipidemia is considered an independent risk factor for renal dysfunction and induces a significant increase in the expression of inflammatory mediators, which can be used to evaluate the degree of renal injury. Baicalin is widely used in traditional Chinese herbal medicine and has multiple pharmacological effects. The present study investigated whether baicalin can attenuate the expression of vascular cell adhesion molecule 1 (VCAM‑1) via a reduction in the expression of monocyte chemoattractant protein‑1 (MCP‑1) and interleukin‑6 (IL‑6) in the kidney of apolipoprotein E (ApoE)‑knockout (KO) mice fed a high cholesterol diet. These mice were used as a model of atherosclerosis and were treated with baicalin (100 mg/kg/day) daily by gavage for a period of 12 weeks. By contrast, wild‑type male C57BL/6J mice were fed a standard diet. Blood samples were obtained from the angular veins of the mice to measure the total cholesterol (TC) and the expression levels of VCAM‑1, MCP‑1 and IL‑6 in the kidney tissues of the mice were analyzed using reverse transcription quantitative polymerase chain reaction and western blot analysis. Following oral administration of baicalin, no significant difference was observed in the TC in the baicalin group compared with the high cholesterol diet control group. The TC was significantly higher in the AopE‑KO mice compared with the wild‑type male C57BL/6J mice. The expression levels of VCAM‑1, MCP‑1 and IL‑6 in the kidney tissues of the baicalin group were lower compared with those in the high cholesterol diet control group. The results suggested that baicalin decreased the expression levels of pro‑inflammatory mediators and prevented kidney dysfunction in the ApoE‑KO mice fed a high cholesterol diet.

Baicalin inhibits proliferation and promotes apoptosis of vascular smooth muscle cells by regulating the�MEG3/p53 pathway following treatment with ox‑LDL

“…In a previous study, baicalin and geniposide inhibited the progression of AS by enhancing the expression of Wnt family member 1 and attenuating the expression of dickkopf-related protein 1 (51). In a high-cholesterol diet, baicalin decreased the expression of monocyte chemoattractant protein 1 and interleukin-6 in the kidneys of ApoE knock out mice (23). Although baicalin has been demonstrated to exhibit a number of biological functions, the underlying mechanism of baicalin-mediated prevention of AS progression by altering lncRNA expression is not well documented.…”

“…Previous studies indicated that baicalin may induce numerous pharmacological effects, including anti-oxidative (19), antitumor (20), anti-inflammatory (21) and antiproliferative (17) functions. Baicalin inhibited the activation of nuclear factor-κB, decreased the expression of pro-inflammatory mediators and prevented renal dysfunction in ApoE knock out mice on high-cholesterol diets, which served an important role in the prevention of AS (22,23). A number of studies reported that p53 serves an important role in the pathogenesis of AS (2,24,25).…”

Promising influences of Scutellaria baicalensis and its two active constituents, baicalin, and baicalein, against metabolic syndrome: A review

“…It has been found that monocyte chemoattractant protein‐1 (MCP‐1) and IL‐6 are significant markers for hyperlipidemia‐induced renal dysfunction (Garibotto et al, 2007). Baicalin (100 mg/kg/day, orally) made a significant decrement in the expression levels of vascular cell adhesion molecule (VCAM)‐1, and MCP‐1, as well as IL‐6 level in the kidney tissue and prevented the renal dysfunction of apolipoprotein E (ApoE)‐knockout mice fed with high cholesterol diet (Liu et al, 2015).…”

“…Baicalin (100 mg/kg/day, orally) made a significant decrement in the expression levels of vascular cell adhesion molecule (VCAM)-1, and MCP-1, as well as IL-6 level in the kidney tissue and prevented the renal dysfunction of apolipoprotein E (ApoE)-knockout mice fed with high cholesterol diet (Liu et al, 2015).…”

Regulatory Mechanisms of Baicalin in Cardiovascular Diseases: A Review

“…In an in vitro study, baicalin was found to decrease monocyte adhesion via reducing the expression of MCP-1, ICAM-1, and VCAM-1 in the presence of high glucose-induced human umbilical vein endothelial cells (HUVECs). Similarly, baicalin had been confirmed to markedly decrease the release of MCP-1, VCAM-1 and IL-6 in the kidney of apolipoprotein E (ApoE)' knockout (KO) mice (Liu et al, 2015). Further, baicalin inhibited the synthesis of neutrophil chemokines and blocked the biological activity of receptors by selectively binding chemokine receptors, thereby inhibiting the migration and aggregation of inflammatory cells and reducing the degree of AS (Li et al, 2000).…”