Ginsenoside Rg1 protects human renal tubular epithelial cells from lipopolysaccharide-induced apoptosis and inflammation damage

Abstract

Ginsenoside Rg1, one of the most notable active components of Panax ginseng, has been widely reported to exert anti-inflammatory actions. This study aimed to reveal whether ginsenoside Rg1 also exhibits beneficial roles against lipopolysaccharide (LPS)-induced apoptosis and inflammation in human renal tubular epithelial cells, and to evaluate the potential role of the component on tubulointerstitial nephritis treatment. HK-2 cells were treated with various doses of ginsenoside Rg1 (0, 50, 100, 150, and 200 μM) in the absence or presence of 5 μg/mL LPS. Thereafter, CCK-8 assay, flow cytometry, western blot, migration assay, reactive oxygen species (ROS) assay, and ELISA were carried out to respectively assess cell viability, apoptosis, migration, ROS activity, and the release of inflammatory cytokines. As a result, ginsenoside Rg1 protected HK-2 cells from LPS-induced injury, as cell viability was increased, cell apoptosis was decreased, and the release of MCP-1, IL-1β, IL-6, and TNF-α was reduced. Ginsenoside Rg1 functioned to HK-2 cells in a dose-dependent manner, and the 150 μM dose exhibited the most protective functions. Ginsenoside Rg1 had no significant impact on cell migration and ROS activity, while it alleviated LPS-induced ROS release and migration impairment. Furthermore, the down-regulations of p-PI3K, p-AKT, and up-regulations of PTEN, p-IκBα, p-p65, Bcl-3 induced by LPS were recovered to some extent after ginsenoside Rg1 treatment. In conclusion, ginsenoside Rg1 protects HK-2 cells against LPS-induced inflammation and apoptosis via activation of the PI3K/AKT pathway and suppression of NF-κB pathway.

The Urinary Angiotensinogen to Urinary Albumin Ratio Reflects Whether the Renin-angiotensin System in the Kidney Is Activated due to Filtration of Plasma Angiotensinogen through the Damaged Glomeruli or the Production of Angiotensinogen in the Proximal Tubules

“…Why the intrarenal RAS activation was increased in patients with tubulointerstitial nephritis is unclear. However, inflammation and reactive oxygen species (ROS) in tubulointerstitial nephritis are well known to be upregulated, and inflammation and ROS augment intrarenal RAS activation (9,(26)(27)(28)(29)(30)(31). For example, Satou et al showed that interleukin-6 (IL-6) augments AGT in primary cultured renal proximal tubular cells (27).…”

Neuroprotective Effects of Ginsenoside-Rg1 Against Depression-Like Behaviors via Suppressing Glial Activation, Synaptic Deficits, and Neuronal Apoptosis in Rats

“…As a result, the activation of NF-κB triggered expression of pro-apoptotic factor genes, which ultimately leads to apoptosis and neural cell death (67). Previous studies have demonstrated that ginsenoside-Rg1 could protect hepatocytes against excessive inflammation and hepatocellular apoptosis via preventing the NF-κB pathway (68–70) and may prevent against acute liver injury by activating Nrf2 signaling pathway in mice (71). Consistently, in the present study, we found that pretreatment of ginsenoside-Rg1 significantly reversed the increased phosphorylation levels of NF-κB P65 subunit, as well as reversed the decreased expression of Nrf2 within the vmPFC of these CUMS rats.…”

Ginsenoside Rg1 and Resveratrol Alleviate Acute Kidney Injury Induced by Cisplatin via Downregulation of Autophagy in Mice

“…Besides autophagy, other mechanisms may contribute to the renoprotective effects of Rg1 and resveratrol. Rg1 could alleviate oxidative stress injury in mice with subacute renal damage induced by d-galactose [27], reduce oxidative stress by inhibiting TGF-β1/Smads signaling pathway in diabetic nephropathy [6], suppress inflammation and apoptosis in LPS-induced HK-2 cells [28], and inhibit apoptotic and fibrotic process partly through inhibition of endoplasmic reticulum stress in rats with unilateral ureteral obstruction [29]. Resveratrol may alleviate renal injury induced by cisplatin via reducing apoptosis of renal tubular cells [30], reducing oxidative stress [31], inhibiting inflammation [32].…”