Correlation analysis of differentially expressed long non-coding RNA HOTAIR with PTEN/PI3K/AKT pathway and inflammation in patients with osteoarthritis and the effect of baicalin intervention

Abstract

Objective This study aims to investigate the correlation of long non-coding RNA HOX transcript antisense RNA (lncRNA HOTAIR) with the PTEN/PI3K/AKT pathway and clinical-related indicators in osteoarthritis (OA) and determine the effect of baicalin intervention. Methods The levels of clinical lipid metabolism indexes and immune-inflammatory indexes in OA patients and normal controls was detected. OA chondrocytes (OA-CHs) were induced with peripheral blood mononuclear cells (PBMCs), followed by baicalin treatment (50 ug/mL). RT-qPCR was performed to measure lncRNA HOTAIR expression. The levels of inflammatory cytokines and adiponectin were detected using ELISA kits. CCK-8 assay was used to assess the viability of CHs. The related protein expression was measured using Western blot analysis. Results LncRNA HOTAIR might act as a biomarker of OA in vivo. LncRNA HOTAIR was positively correlated with TC, hs-CRP, IgA, TNF-α, and VAS score. Overexpression of lncRNA HOTAIR in vitro inhibited cell proliferation, reduced IL-10 and PTEN expression, but augmented TNF-α, p-PI3K, and p-AKT proteins in OA-CHs stimulated by OA-PBMCs. The changes of above indexes were also observed in OA-CHs stimulated by OA-PBMCs treated with si-lncRNA HOTAIR or baicalin, implying the synergistic effects of baicalin and lncRNA HOTAIR silencing on OA. Conclusions Conclusively, lncRNA HOTAIR was highly expressed in OA-CHs, which facilitated OA inflammatory responses by orchestrating inflammatory cytokines and the PTEN/PI3K/AKT pathway. Baicalin exerted therapeutic effects by inhibiting the expression of lncRNA HOTAIR, decreasing the protein levels of p-PI3K and p-AKT, and increasing the protein levels of PTEN, APN, and ADIPOR1.

Global research trends and hotspots of PI3K/Akt signaling pathway in the field of osteoarthritis: A bibliometric study

“…Conclusively, lncRNA HOTAIR was highly expressed in OA-chondrocytes, which facilitated OA inflammatory responses by orchestrating inflammatory cytokines and the PTEN/PI3K/AKT pathway. [ 52 ] Meng et al [ 53 ] studied the connections of markers to chondrocyte autophagy and apoptosis in OA were also comprehensively explored in vitro using molecular biology approaches. PDK1 was finally identified as a diagnostic marker for OA.…”

LncRNA-mediated cartilage homeostasis in osteoarthritis: a narrative review

“…By inhibiting the expression of the lncRNA HOTAIR , decreasing the protein levels of p-PI3K and p-AKT, and increasing the protein levels of PTEN, APN, and ADIPOR1, Chen’s group discovered that baicalin plays a therapeutic role ( 72 ).…”

Osteoarthritis in the Elderly Population: Preclinical Evidence of Nutrigenomic Activities of Flavonoids

“…Flavanones , also known as dihydroflavones, lack a double bond between carbons 2 and 3, which are present in flavones and flavonols. We have found nine manuscripts regarding four molecules: baicalin, naringenin (NAR), sappanone A, wogonoside [ 43 , 44 , 45 , 46 , 47 , 48 , 49 , 50 , 51 ]. Baicalin is extracted from Scutellaria baicalensis Georgi, and exhibited anti-OA activities.…”

“…In particular, lncRNA HOX transcript antisense RNA (HOTAIR) was indicated as being higher in OA chondrocytes to such an extent that it is considered a biomarker of OA in vivo. These same authors also have demonstrated that baicalin inhibits lncRNA HOTAIR expression, diminishing the protein levels of p-PI3K and p-AKT, and growing the protein levels of PTEN, OPN, and ADIPOR1 [ 43 ]. Other authors, by performing in vivo and in vitro analyses, have demonstrated that baicalin lessened OA progression in vivo and showed a chondroprotective effect in vitro by quashing chondrocyte ferroptosis, which, in turn, can reduce OA-related pain sensitivity in OA mice.…”