Ginsenoside Rg1 inhibits nucleus pulposus cell apoptosis, inflammation and extracellular matrix degradation via the YAP1/TAZ pathway in rats with intervertebral disc degeneration.

PURPOSE: Intervertebral disc degeneration (IDD) is one of the main causes of low back pain, which not only affects patients' life quality, but also places a great burden on the public health system. Recently, ginsenoside Rg1 has been found to act in IDD; however, the mechanism is still unclear. The purpose of this study is to explore the function of ginsenoside Rg1 and its molecular mechanism in IDD. METHODS: The rat model of IDD and nucleus pulposus (NP) experimental groups treated with ginsenoside Rg1 was constructed for investing the role of ginsenoside Rg1 in IDD rats. In the in vitro and in vivo study, the histological morphological changes, motor threshold (MT), inflammatory factors, oxidative stress, apoptosis and expression of the YAP1/TAZ signaling pathway-related proteins of the intervertebral discs (IVD) were measured by histological staining, mechanical and thermal stimulation, ELISA, qRT-PCR, flow cytometry, and western blot, respectively. RESULTS: Ginsenoside Rg1 significantly increased the threshold for mechanical and thermal stimulation and alleviated histological changes in IDD rats. Ginsenoside Rg1 had a significant inhibitory effect on the secretion level of inflammatory factors, redox activity, extracellular matrix (ECM) degradation in IVD tissue and NP cells, and apoptosis in NP cells. Further investigation revealed that ginsenoside Rg1 significantly inhibited the expression of YAP1/TAZ signaling pathway-related proteins. Additionally, the above inhibitory effect of ginsenoside Rg1 on IDD progression was concentration-dependent, that is, the highest concentration of ginsenoside Rg1 was most effective. CONCLUSION: Ginsenoside Rg1 inhibits IDD progression by suppressing the activation of YAP1/TAZ signaling pathway. This means that ginsenoside Rg1 has the potential to treat IDD.

Temporal retinal thinning might be an early diagnostic indicator in male pediatric X-linked Alport syndrome.

AIM: To evaluate temporal retinal thinning changes in retinal layers using spectral-domain optical coherence tomography (SD-OCT) in pediatric X-linked Alport syndrome (XLAS) patients. METHODS: A retrospective case-control study. SD-OCT scans of pediatric patients diagnosed with XLAS and age- and sex-matched healthy control participants were reviewed. Automated segmentation of SD-OCT scans was induced to analyze the retinal thickness (RT) of different layers. The temporal thinning index (TTI) was calculated for each layer and compared between the patients and the control group. RESULTS: Forty-three pediatric XLAS patients and 60 healthy controls were included. Temporal retinal thinning was present in 33 patients (76.74%), while 28 patients (65.11%) had severe pathological temporal retinal thinning and 5 patients (11.63%) had moderate thinning. The temporal inner sector RT (P<0.0001), the temporal outer sector RT (P<0.0001), and the nasal outer sector RT (P=0.0211) were significantly thinner in the XLAS male patients. The TTI of the total retina was significantly higher in the XLAS group than in the control group (P<0.0001). The TTI of the inner retina layers (P<0.0001), ganglion cell layer (P<0.0001), inner plexiform layer (P<0.0001), inner nuclear layer (P<0.0001), and outer nuclear layer (P<0.0001) were significantly higher in the XLAS group. The central RT of the XLAS group was significantly thinner than that of the control group (P<0.0001). CONCLUSION: Temporal retinal thinning appears early in XLAS patients, especially in male patients. The thinning is mainly caused by structural abnormalities of the inner retina. This suggests that temporal retinal thinning could be helpful for the early diagnosis and follow-up of XLAS with noninvasive SD-OCT examination.