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Microplastics (MPs) pollution has received widespread attention in recent years as the use of plastics continues to increase. However, currently no studies have reported the finding of MPs in human uterine fibroids (UFs) and myometrium tissues. In this study, UFs tissues (n = 48) and myometrium tissues (n = 40) from 48 patients and myometrium tissues (n = 8) from healthy population were collected. Following digestion of the samples by 10% KOH and 30% H 2 O 2 , MPs were analyzed qualitatively and quantitatively using Raman spectroscopy. The 16 UFs and myometrium tissue samples contained an average of 1.5 ± 1.17 MP particles per gram of tissue. Notably, the abundance of MPs in the UFs tissues (2.13 ± 1.17 particles per gram) was higher than in the myometrium tissues (0.88 ± 0.78 particles per gram). In the same cohort of individuals with UFs, the quantities of MPs detected in the affected UFs tissue (2.63 ± 1.77 particles per gram) exceeded those detected in healthy tissue (1.08 ± 0.93 particles per gram), particularly in elderly patients. A correlation was observed between elevated MP levels and frequent consumption of takeout meals and bottled water among patients, indicating that MP ingestion through food sources might have contributed to the increased abundance and variety of MPs within UFs. Furthermore, UFs increased in size with higher concentrations of MPs, which may have been related to elevated levels of MPs-induced hormones. This study provides new insights into the assessment of the relationship between exposure to MPs and human disease risk. In this study, the authors, through the integration of Raman spectroscopy and uterine fibroids (UFs) microscopy, achieve a comprehensive assessment of the pathological alterations in UFs. This is the first time that microplastics (MPs) particles have been identified in UFs and myometrium tissues. This study suggests that higher concentrations of MPs in diseased tissues compared to normal tissues. [Display omitted] • Microplastics are detected in female uterine fibroids tissues using Raman. • PE, PP, PE-co-PP are the dominant polymer types of microplastics. • The concentration of microplastics in uterine fibroids tissue increased with age. • Dietary habits may affect the levels and diversity of microplastics. • 5. The presence of microplastics may be associated with the growth of uterine fibroids. [ABSTRACT FROM AUTHOR]

Currently, there are no specific drugs or targets available for the treatment of tendinopathy. However, inflammation has recently been found to play a pivotal role in tendinopathy progression, thereby identifying it as a potential therapeutic target. Carpaine (CA) exhibits potential anti-inflammatory pharmacological properties and may offer a therapeutic option for tendinopathy. This study aimed to investigate the effectiveness of CA in addressing tendinopathy and uncovering its underlying mechanisms. Herein, the efficacy of CA by local administration in vivo in comparison to the first-line drug indomethacin was evaluated in a mouse collagenase-induced tendinopathy (CIT) model. Furthermore, IL-1β induced a simulated pathological inflammatory microenvironment in tenocytes to investigate its underlying mechanisms in vitro. Further confirmation experiments were performed by overexpressing or knocking down the selective targets of CA in vivo. The findings demonstrated that CA was dose-dependent in treating tendinopathy and that the high-dose group outperformed the first-line drug indomethacin. Mechanistically, CA selectively bound to and enhanced the activity of the E3 ubiquitin ligase LRSAM1 in tendinopathy. This effect mediated the ubiquitination of p65 at lysine 93, subsequently promoting its proteasomal degradation. As a result, the NF-κB pathway was inactivated, leading to a reduction in inflammation of tendinopathy. Consequently, CA effectively mitigated the progression of tendinopathy. Moreover, the LRSAM1 overexpression demonstrated effectiveness in mitigating the tendinopathy progression and its knockdown abolished the therapeutic effects of CA. CA attenuates the progression of tendinopathy by promoting the ubiquitin-proteasomal degradation of p65 via increasing the enzyme activity of LRSAM1. The exploration of LRSAM1 has also unveiled a new potential target for treating tendinopathy based on the ubiquitin-proteasomal pathway. [Display omitted] [ABSTRACT FROM AUTHOR]