Triptolide is the main bioactive constituent isolated from the Chinese herb Tripterygium wilfordii Hook F., which possesses a variety of pharmacological properties. MicroRNAs (miRNAs/miRs) are short non-coding RNAs that regulate gene expression post-transcriptionally. miRNAs are implicated in several intracellular processes, whereby their dysregulation contributes to pathogenesis of various diseases. Thus, miRNAs have great potential as biomarkers and therapeutic targets for diseases, and are implicated in drug treatment. Previous studies have reported that specific miRNAs are targeted, and their expression levels can be altered following exposure to triptolide. Thus, miRNAs are emerging as crucial mediators in the pharmacological activities of triptolide. The present review summarizes current literature on miRNAs as target molecules in the pharmacological activities of triptolide, including antitumor, anti-inflammatory, immunosuppressive, renal protective, cardioprotective, antiangiogenesis activities and multiorgan toxicity effects. In addition, the diverse signaling pathways involved are discussed to provide a comprehensive understanding of the underlying molecular mechanisms of triptolide in the regulation of target miRNAs.
Celastrol, a natural compound extracted from the traditional Chinese medicinal herb Tripterygium wilfordii Hook F, possesses broad-spectrum pharmacological properties. Autophagy is an evolutionarily conserved catabolic process through which cytoplasmic cargo is delivered to the lysosomes for degradation. Autophagy dysregulation contributes to multiple pathological processes. Therefore, targeting autophagic activity is a promising therapy for various diseases, as well as a drug-development strategy. According to previous studies, autophagy is specifically targeted and may be altered in response to celastrol treatment, highlighting that autophagy modulation is an important mechanism underlying the therapeutic efficacy of celastrol for the treatment of various diseases.The present study summarizes the currently available information regarding the role of autophagy in the effect of celastrol to exert anti-tumor, anti-inflammatory, immunomodulatory, neuroprotective, anti-atherosclerosis, anti-pulmonary fibrosis and anti-macular degeneration activities. The diverse signaling pathways involved are also analyzed to provide insight into the mechanisms of action of celastrol and thereby pave the way for establishing celastrol as an efficacious autophagy modulator in clinical practice. Contents 1. Introduction 2. An overview of autophagy 3. Autophagy regulation by celastrol 4. Mechanisms underlying autophagy modulation by celastrol 5. Conclusion and future perspectives
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