Notes

Molecular cloning, depiction, as well as advancement research into the luciferase family genes via a few sympatric sister fireflies (Lampyridae: Lampyrinae, Diaphanes).
The three dihydroxystilbenes also suppressed COX-2 expression in colon tumors (in vivo). The results obtained also revealed that the three dihydroxystilbenes inhibited PD-1 elevations in M2-THP-1 macrophages (in vitro). Therefore, the inhibition of AOM/DSS-induced colon carcinogenesis and colon tumor growth by 2,3-, 3,4-, and 4,4'-dihydroxystilbenes appears to be due to the suppression of M2 TAM differentiation and activation and PD-1 expression (immunosuppression) via reductions in COX-2 expression levels in the colon tumor microenvironment.Geniposide (GE) can effectively inhibit diabetic nephropathy (DN), but its mechanism is unclear. The objective of this study was to explore the antidiabetic nephropathy effects of GE both in high fat diet/streptozotocin-induced DN mice and in high glucose-induced podocyte model. Renal function in DN mice was evaluated by levels of serum creatinine (Scr) and blood urea nitrogen (BUN). Renal inflammation was appraised by pro-inflammatory cytokines Tumor necrosis factor α (TNF-α), Interleukin 6 (IL-6) and IL-1β via ELISA assay. Renal histopathology analysis was conducted via hematoxylin and eosin, Masson and periodic acid-silver metheramine staining. Cellular viability was measured by Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay. Moreover, the related proteins p-NF-κB, ASC, Cleave-IL-1β, NLRP3, Cleave-Caspase-1 and GSDMD-N in AMPK/SIRT1/NF-κB pathway were assayed by Western blotting. In order to further investigate the effects of GE on podocytes, we also assessed these protein levels in AMPK/SIRT1/NF-κB pathway after siRNA-AMPK intervention by Western blotting. GE alleviated renal dysfunction as evidenced by decreased levels of Scr, BUN, TNF-α, IL-6 and IL-1β. Histological examination revealed GE effectively attenuated kidney damage, including glomerular basement membrane thickening and inflammatory cells infiltration. AMPK, p-AMPK and SIRT1 levels were obviously decreased both in DN mice and in podocyte model, but GE reversed these changes. The protein expressions in APMK/SIRT1/NF-κB pathway were significantly decreased by GE treatment. These results suggested that GE could efficiently block oxidative stress and inflammatory responses accompanied with pyroptosis, thus inhibiting the development of DN, and its mechanism might be related to APMK/SIRT1/NF-κB pathway.SARS-CoV-2 has devastated the world with its rapid spread and fatality. The researchers across the globe are struggling hard to search a drug to treat this infection. Understanding the time constraint, the best approach is to study clinically approved drugs for control of this deadly pandemic of COVID 19. The repurposing of such drugs can be supported with the study of molecular interactions to enhance the possibility of application. The present work is a molecular docking study of proteins responsible for viral propagation namely 3Clpro, Nsp10/16, Spike protein, SARS protein receptor binding domain, Nsp 9 viral single strand binding protein and viral helicase. The protein through virus enters the host cell-human angiotensin-converting enzyme 2 (ACE2) receptor, is also used as a target for molecular docking. The docking was done with most discussed drugs for SARS-CoV-2 like Ritonavir, Lopinavir, Remdesivir, Chloroquine, Hydroxychloroquine (HCQ), routine antiviral drugs like Oseltamivir and Ribavirin. In addition, small molecules with anti-inflammatory actions like Mycophenolic acid (MPA), Pemirolast, Isoniazid and Eriodictyol were also tested. The generated data confirms the potential of Ritonavir, Lopinavir and Remdesivir as a therapeutic candidate against SARS-CoV-2. It is observed that Eriodictyol binds to almost all selected target proteins with good binding energy, suggesting its importance in treatment of COVID 19. Molecular interactions of Ritonavir, Lopinavir and Remdesivir against SARS-CoV-2 proteins enhanced their potential as a candidate drug for treatment of COVID-19. Eriodictyol had emerged as a new repurposing drug that can be used in COVID-19.Intraocular pressure (IOP) lowering in glaucomatous eyes is currently achieved mainly by improved aqueous outflow via alternate drainage pathways. However, the focus is now shifting to trabecular meshwork (TM), the site or major pathological changes including increased extracellular matrix (ECM) deposition and reduced matrix metalloproteinases (MMPs) secretion by TM cells. Trans-resveratrol was previously shown to lower IOP and reduce ECM deposition; however, the mechanisms of action remain unclear. Therefore, we determined the effect of trans-resveratrol on MMP-2 and -9 expression by human TM cells (HTMCs) in the presence of dexamethasone and whether it also affects adenosine A1 receptors (A1AR) expression and nuclear factor kappa B (NFkB) activation. We observed that trans-resveratrol, 12.5 μM, increased MMP-2 and -9 protein expression by HTMCs despite exposure to dexamethasone (1.89- and 1.53-fold, respectively; P less then 0.001). Further it was observed that trans-resveratrol increases A1AR expression in HTMC in the presence of dexamethasone (1.55-fold; P less then 0.01). Trans-resveratrol also increased NFkB activation in the presence of dexamethasone and A1AR antagonist (P less then 0.01 versus dexamethasone group). check details These effects of trans-resveratrol were associated with increased MMP -2 and -9 expression. It could be concluded that trans-resveratrol prevents dexamethasone-induced reduction in MMP-2 and -9 secretion by NFkB activation in HTMCs. This effect of trans-resveratrol is likely to involve increased A1AR expression.Bufadienolides are cardioactive C24 steroids with an α-pyrone ring at position C17. In the last ten years, accumulating studies have revealed the anticancer activities of bufadienolides and their underlying mechanisms, such as induction of autophagy and apoptosis, cell cycle disruption, inhibition of angiogenesis, epithelial-mesenchymal transition (EMT) and stemness, and multidrug resistance reversal. As Na+/K+-ATPase inhibitors, bufadienolides have inevitable cardiotoxicity. Short half-lives, poor stability, low plasma concentration and oral bioavailability in vivo are obstacles for their applications as drugs. To improve the drug potency of bufadienolides and reduce their side effects, prodrug strategies and drug delivery systems such as liposomes and nanoparticles have been applied. Therefore, systematic and recapitulated information about the antitumor activity of bufadienolides, with special emphasis on the molecular or cellular mechanisms, prodrug strategies and drug delivery systems, is of high interest.
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