Nanoencapsulation of extracts and isolated compounds of plant origin and their cytotoxic effects on breast and cervical cancer treatments: Advantages and new challenges.

This review analyzes the current progress in loaded nanoparticles (NPs) of plant extracts or isolated antineoplastic compounds used in breast and cervical cancer treatments. Also, it provides a comprehensive overview of the contributions made by traditional medicine and nanomedicine to the research of two of the most prevalent types of cancer in women worldwide: breast and cervical cancer. Searches were conducted in electronic databases to gather relevant information related to the biological activity of the NPs, which were meticulously reviewed. Nanomedicine has advanced to incorporate plant compounds including their crude extracts, in the preparation of NPs. The most used method is green synthesis, whose most outstanding advantages, is the reduced preparation time, and the variety of results that can be obtained depending on the reaction times, pH, temperature, and concentration of both the bio-reducing agent and the compound or plant extract. Most of the studies focus on evaluating crude extracts with high polarity, such as aqueous, alcoholic, and hydroalcoholic extracts. In conclusion, exploring the use of organic compounds is considered an area of opportunity for further research and future perspectives. Most of the analyzed studies were conducted using in vitro assays, highlighting the relatively recent nature of this field. It is expected that future research will involve more in vivo assays, particularly focusing on isolated cell lines representing the most difficult-to-treat types of cancer, such as triple-negative breast cancer like MDA-MB-231. Notably the MCF-7 cell line is one of the most used, while limited studies were found concerning cervical cancer.

CDNF overexpression prevents motor-cognitive dysfunction by intrastriatal CPP-based delivery system in a Parkinson's disease animal model.

Parkinson's disease (PD) is characterized by the loss of dopaminergic neurons in the substantia nigra pars compact (SNpc), and no effective treatment has yet been established to prevent PD. Neurotrophic factors, such as cerebral dopamine neurotrophic factor (CDNF), have shown a neuroprotective effect on dopaminergic neurons. Previously, we developed a cell-penetrating-peptide-based delivery system that includes Asn194Lys mutation in the rabies virus glycoprotein-9R peptide (mRVG9R), which demonstrated a higher delivery rate than the wild-type. In this study, using a mouse PD-like model, we evaluated the intrastriatal mRVG9R-KP-CDNF gene therapy through motor and cognitive tests and brain cell analysis. The mRVG9R-KP-CDNF complex was injected into the striatum on days 0 and 20. To induce the PD-like model, mice were intraperitoneally administered Paraquat (PQ) twice a week for 6 weeks. Our findings demonstrate that mRVG9R-KP-CDNF gene therapy effectively protects brain cells from PQ toxicity and prevents motor and cognitive dysfunction in mice. We propose that the mRVG9R-KP-CDNF complex inhibits astrogliosis and microglia activation, safeguarding dopaminergic neurons and oligodendrocytes from PQ-induced damage. This study presents an efficient CDNF delivery system, protecting neurons and glia in the nigrostriatal pathway from PQ-induced damage, which is known to lead to motor and cognitive dysfunction in neurodegenerative diseases such as PD.

Histopathological, ultrastructural, and biochemical traits of apoptosis induced by peroxisomicine A1 (toxin T-514) from Karwinskia parvifolia in kidney and lung.

Peroxisomicine A1 (PA1) is a toxin isolated from the Karwinskia genus plants whose target organs are the liver, kidney, and lung. In vitro studies demonstrated the induction of apoptosis by PA1 in cancer cell lines, and in vivo in the liver. Apoptosis has a wide range of morphological features such as cell shrinkage, plasma membrane blistering, loss of microvilli, cytoplasm, and chromatin condensation, internucleosomal DNA fragmentation, and formation of apoptotic bodies that are phagocytized by resident macrophages or nearby cells. Early stages of apoptosis can be detected by mitochondrial alterations. We investigated the presence of apoptosis in vivo at the morphological, ultrastructural, and biochemical levels in two target organs of PA1: kidney and lung. Sixty CD-1 mice were divided into three groups (n = 20): untreated control (ST), vehicle control (VH), and PA1 intoxicated group (2LD50). Five animals of each group were sacrificed at 4, 8, 12, and 24 h post-intoxication. Kidney and lung were examined by morphometry, histopathology, ultrastructural, and DNA fragmentation analysis. Pre-apoptotic mitochondrial alterations were present at 4 h. Apoptotic bodies were observed at 8 h and increased over time. TUNEL positive cells were detected as early as 4 h, and the DNA ladder pattern was observed at 12 h and 24 h. The liver showed the highest value of fragmented DNA, followed by the kidney and the lung. We demonstrated the induction of apoptosis by a toxic dose of PA1 in the kidney and lung in vivo. These results could be useful in understanding the mechanism of action of this compound at toxic doses in vivo.