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Garcinia indica (Kokum) and Ilex aquifolium (European Holly)
Published in Azamal Husen, Herbs, Shrubs, and Trees of Potential Medicinal Benefits, 2022
Dicson Sheeja Malar, Mani Iyer Prasanth, Tewin Tencomnao, James Michael Brimson, Anchalee Prasansuklab
Ethanol extract of leaves of I. aquifolium inhibited leukotriene biosynthesis and lipid peroxidation in bovine Polymorphonuclear neutrophil leukocyte indicating the anti-inflammatory properties (Müller et al., 1998). UA attenuated allergic inflammation by inhibiting FcεRI-mediated degranulation of mast cells (Dhakal et al., 2021). Upon autoimmune thyroiditis stimulation in Nthy-ori 3-1 cells by inhibiting MALAT1/miR-206/PTGS1 network and NF-κB signaling pathway (Mou et al., 2021). Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) regulates inflammatory cytokine production and the aberrant expression of which is associated with inflammatory diseases (Li et al., 2020a; Masoumi et al., 2019). UA also protected chondrocytes from TNF-α injury by suppressing MMP13, IL-1β, IL-6, and PTGS2 along with the inhibition of NF-κB/NLRP3 inflammasome pathway (Wang et al., 2020). UA alleviates LPS-induced macrophage inflammation and atherogenesis in mice by suppressing cytokine production and enhancing autophagy (Leng et al., 2016). Similarly, UA exerted anti-inflammatory potential against Mycobacterium tuberculosis and concanavalin-A treatment in RAW264.7 cells through the inhibition of TNF‑α, IL‑1β, and IL‑6 (Zerin et al., 2016).
Bone Regeneration Effect of Cassia occidentalis Linn. Extract and Its Isolated Compounds
Published in Brijesh Kumar, Vikas Bajpai, Vikaskumar Gond, Subhashis Pal, Naibedya Chattopadhyay, Phytochemistry of Plants of Genus Cassia, 2021
Brijesh Kumar, Vikas Bajpai, Vikaskumar Gond, Subhashis Pal, Naibedya Chattopadhyay
Besides the preventive/therapeutic effects of quercetin in osteoporotic conditions (OVX-induced or GC-induced), a large number of reports exist on the joint-protective effects of quercetin in a variety of preclinical models of RA and OA. In human RA-derived FLS cells which are the major pathogenic mediator of RA, quercetin suppressed IL-17-induced RANKL production and phosphorylation of mTOR, ERK and IκB-α, which suggested mitigation of inflammatory and bone resorptive outcomes. Furthermore, the IL-17-induced osteoclastogenesis from human CD14+ monocytes was attenuated by quercetin. When the monocytes were cocultured with RA-FLS prestimulated with IL-17, the presence of quercetin significantly attenuated the osteoclast differentiation. Also, the osteoclastic differentiation of CD14+ cells in the presence of Th17 cells was suppressed. Finally, quercetin decreased Th17 cells differentiation without affecting the regulatory T (Treg) cells (Kim et al., 2019). In FLS of RA patients, quercetin induced apoptosis, through the upregulation of a long non-coding RNA (lncRNA), metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) (Pan et al., 2016). These reports suggest that quercetin targets FLS, the major cell type involved in RA pathogenesis from multiple directions and thus showing potential in the treatment of this disease. Accordingly, in a double-blind randomized clinical trial in women with RA, 500 mg quercetin supplementation daily for 8 weeks significantly decreased early morning stiffness, morning pain, after-activity pain, disease activity score-28 (DAS-28) and plasma hs-TNFa compared to the placebo group (Javadi et al., 2017).
Nanoparticles for Cardiovascular Medicine: Trends in Myocardial Infarction Therapy
Published in Harishkumar Madhyastha, Durgesh Nandini Chauhan, Nanopharmaceuticals in Regenerative Medicine, 2022
In addition to MSCs, pluripotent embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs) are attractive sources for stem cell-mediated therapies. Further to this, iPSCs and other pluripotent stem cells (PSCs) can be forced to differentiate into cardiovascular progenitors and other cardiac cells with relative ease and reproducibility. The efficacy of PSC-derived cardiac cell-secreted exosomes in the repair of MI has started to come to light. Wu et al. reported the cardioprotective effects of exosomes secreted by ESC-derived cardiac progenitor cells (Wu et al. 2020a). Intramyocardial injection of exosomes/extracellular vesicles into acutely infracted mouse hearts significantly improved cardiac function, reduced fibrosis, and improved vascularisation and cardiomyocyte survival at infarct border zones. The researchers revealed that a high abundance of the long noncoding RNA, MALAT1, was present and upregulated in the infarcted myocardium and cardiomyocytes treated with exosomes. MALAT1 expression improved cell viability, while its knockdown inhibited exosome-promoted proangiogenic activities, through targeting miR-497. Santoso et al. harvested exosomes from iPSCs that had differentiated into contractile cardiomyocytes (Santoso et al. 2020). The iPSC-derived cardiomyocyte-secreted exosomes preserved cardiac function, myocyte viability, and exerted antiapoptotic effects in mouse MI models. Furthermore, exosomes upregulated autophagy activity to maintain cardiac homeostasis. The researchers implicated autophagic flux impairment as a key characteristic of ischemia, and that it could be restored by exosome treatment. Gao et al. compared intramyocardial injection of a mixture of iPSC-derived cardiomyocyte, endothelial cell, and smooth muscle cell exosomes (2:1:1 ratio) into the pig models of MI (Gao et al. 2020). Measurements of myocardial function and bioenergetics were improved, whilst myocardial hypertrophy and fibrosis were ameliorated in MI regions at 1-month postexosome injection, suggesting an attractive method of harvesting high yields of exosomes to provide acellular therapeutic options for MI. The simultaneous harvest of exosomes from multiple cardiac cell types has been revealed to be a promising source of abundant yields of therapeutic exosomes that exert cardioprotective effects. Cardiospheres are self-assembled multicellular constructs that form after cellular outgrowth from cardiac explants on a nonadhesive substrate. Vandergriff et al. harvested exosomes from cardiospheres and conjugated the exosomes to cardiac homing peptide (peptide sequence CSTSMLKAC) (Vandergriff et al. 2018). The researchers demonstrated increased retention of the exosomes within the MI heart in rat I/R injury models, which was accompanied by decreased infarct size and fibrosis, increased cellular proliferation, and enhanced angiogenesis.
The MALAT1-breast cancer interplay: insights and implications
Published in Expert Review of Molecular Diagnostics, 2023
MALAT1 is a lncRNA that is expressed at high levels in the genome, with a length of about 8,000 nucleotides. It is the first lncRNA identified to be linked with metastasis and survival in NSCLC. Despite its large size, MALAT1 lacks an open reading frame and is thus not translated into a protein in vitro. Rather, it affects how genes are expressed and changes primary transcripts in a similar manner across mammals [13]. Several types of cancer in humans have been linked to mutations in MALAT1, including lung [14,15], breast [16,17], bladder, osteosarcoma [18,19], colorectal [20,21], and liver cancer [22,23]. MALAT1 has been shown to localize to nuclear speckles through in vitro studies [24]. Additionally, knockdown experiments have revealed that it modulates alternative pre-messenger RNA splicing [25]. Further tests indicated no significant differences between Malat1 knockout mice and wild-type mice in terms of phenotypic changes. The deletion of Malat1 did not affect the expression of genes, nuclear speckles, splicing factors, or alternative pre-mRNA splicing in mouse tissues [26,27].
Long Non-coding RNA MALAT1 Alleviates the Elevated Intraocular Pressure (Eiop)-induced Glaucoma Progression via Sponging miR-149-5p
Published in Current Eye Research, 2021
Linling Wang, Jin Gong, Junling Wang, Jing Dan, Ping Wang
Long non-coding RNAs (lncRNAs), a type of non-coding RNAs with more than 200 nucleotides (nt) in length, have been reported to regulate target gene expression at the transcriptional, posttranscriptional and the epigenetic level.8,9 Emerging evidence showed that many lncRNAs were aberrantly expressed in glaucoma model, such as TUG1,10 GAS5.11 LncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1, also named as NEAT2) is located on human chromosome 11q13.1.12 Previous studies indicated that MALAT1 was dysregulated in Parkinson’s disease.13,14 However, the mechanism of MALAT1 in glaucoma remains unclear.
LncRNA MALAT1 improves cerebral ischemia-reperfusion injury and cognitive dysfunction by regulating miR-142-3p/SIRT1 axis
Published in International Journal of Neuroscience, 2023
Shengxi Meng, Bing Wang, Wentao Li
MALAT1 is a non-coding RNA that is predominantly expressed in the nucleus and is highly conserved. MALAT1 was originally found to be overexpressed in tumor tissue samples and involved in the regulation of tumor cell survival and metabolism [5]. Zhang et al. [6] showed that MALAT1 is a highly up-regulated in microvascular endothelial cells after cerebral ischemic. Zhang et al. [7] proposed that MALAT1 plays an important protective role in cerebral ischemic injury by promoting the survival of brain microvascular endothelial cells and inhibiting endothelial inflammation. However, the role of MALAT1 in CI/R and related mechanisms remain to be further explored.