Echinacoside promotes the proliferation of human renal tubular epithelial cells by blocking the HBX/TREM2‑mediated NF‑κB signalling pathway
- Yufan Zhang
- Qinfang Wu
- Limin Zhong
- Lei Wang
- Dongwei Gong
Affiliations: Department of Traditional Chinese Medicine, Yangpu District Kongjiang Hospital, Shanghai 200093, P.R. China, Department of Paediatrics, Yangpu District Kongjiang Hospital, Shanghai 200093, P.R. China, Department of Pharmacy, Yangpu District Kongjiang Hospital, Shanghai 200093, P.R. China, Department of Rehabilitation, Yangpu District Kongjiang Hospital, Shanghai 200093, P.R. China, Department of Surgery, Yangpu District Kongjiang Hospital, Shanghai 200093, P.R. China
- Published online on: June 2, 2020 https://doi.org/10.3892/mmr.2020.11201
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Hepatitis B virus X (HBX) protein is required for the replication of HBV and plays a role in the progression of hepatitis in humans. However, the underlying function of HBX during HBV‑induced chronic glomerulonephritis (HBV‑GN) is unknown. Echinacoside (ECH) is a phenylethanoid glycoside from the Cistanche genus, which possesses strong antiapoptosis and neuroprotective activities. In the present study, the function of HBX and the relationship between HBX and ECH in human renal tubular epithelial cells (RTECs; HK‑2 cell line) were explored. Reverse transcription‑quantitative PCR and western blot analyses were used to quantify the mRNA and protein expression levels of HBX in HK‑2 cells, respectively. The Cell Counting Kit‑8 assay was performed to analyse cell proliferation. Flow cytometry analysis was used to determine the rate of apoptosis. HBX showed antiproliferative and proapoptotic effects in HK‑2 cells and was positively associated with triggering receptor expressed on myeloid cells 2 (TREM2) expression. Furthermore, ECH disrupted the function of HBX in HK‑2 cells, functioning as an HBX suppressor. Moreover, a specific NF‑κB inhibitor, PDTC, was used to further examine the relationship between HBX and NF‑κB. The results suggested that NF‑κB was involved in the HBX/TREM2 signaling pathway and negatively regulated TREM2 expression in RTECs. The present study provided novel insights into the function of HBX, and also indicated the potential value of ECH as a therapeutic agent for HBV‑GN.