Salman Islam

Artemia salina, crustaceans of class Branchiopoda and order Anostraca, are living and reproducing only in highly saline natural lakes and in other reservoirs where sea water is evaporated to produce salt. Artemia salina eggs can be purchased from pet stores, where they are sold as tropical fish food and a ready source for hatching shrimp. In the current study, methanolic crude extracts and various fractions of Artemia salina eggs extracted in other solvents were tested for effects on cell viability of human colorectal cancer cells (HCT116) and melanoma cells (B16F10) using an MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay. A methanolic crude extract of eggs was obtained by cold maceration, followed by fractionation to obtain hexane, chloroform, ethyl acetate, n-butanol, and aqueous fractions. The methanolic crude extract decreased cell viability of HCT-116 and B16F10 cell lines at higher concentrations. The other fractions were evaluated using a cell viability assay, and chloroform and hexane showed the highest activity at significantly lower concentrations than did the methanolic fraction. Full scan profiles of the methanolic crude extract and the chloroform and hexane fractions were obtained by gas chromatography mass spectrometry (GC-MS), and the resultant compounds were identified by comparing their spectral data to those available in spectral matching libraries. ROS generation assay, flow cytometry, and western blot analysis provided supporting evidence that the hexane and chloroform fractions induced cell death in HCT116 and B16-F10 cell lines. All fractions were further tested for antibacterial activity against Pseudomonas aeruginosa, among which the hexane fraction showed the highest zone of inhibition on LB nutrient agar plates. This study demonstrated promising anticancer and antibacterial effects of Artemia salina egg extracts. Our results suggest that pure bioactive compounds obtained from Artemia salina eggs can provide new insights into the mechanisms of colon and skin cancer, as well as Pseudomonas aeruginosa inhibition.

This study reports the fabrication of porogen-induced, surface-modified, 3-dimensionally microporous regenerated bacterial cellulose (rBC)/gelatin (3DMP rBC/G) scaffolds for skin regeneration applications. Round shaped gelatin microspheres (GMS), fabricated using a water-in-oil emulsion (WOE) method, were utilized as the porogen. The dissolution of GMS from the solution casted BC scaffolds led to surface-modified microporous rBC. The scaffolds were characterized using field emission scanning electron microscopy (FE-SEM) and elemental analysis. FE-SEM analysis confirmed the regular microporosity of the 3DMP rBC/G scaffolds, while elemental analysis confirmed the successful surface modification of cellulose with gelatin. In vitro tests showed good adhesion and proliferation of human keratinocytes (HaCaT) on the 3DMP rBC/G scaffolds during 7 days of incubation. Confocal microscopy showed penetration of HaCaT cells into the scaffolds, up to 300 μm in depth. In vivo wound healing and skin regeneration experiments, in experimental mice, showed complete skin regeneration within 2 weeks. The wound closure efficacy of the 3DMP rBC/G scaffolds was much higher (93%) than that of the control (47%) and pure BC-treated (63%) wounds. These results indicated that our 3DMP rBC/G scaffolds represent future candidate materials for skin regeneration applications.

Background: Cellulose being the most abundant polymer has been widely utilized in multiple applications. Its impressive nanofibril arrangement has provoked its applications in numerous fields. Recent trends have been shifted to produce composites of nanocellulose for numerous applications among which the most important ones are its use in medical and environmental prospective. This review has basically focused the development of nanocellulose composites and its applications in resolving environmental hazards. Methods: We have reviewed large number of research and review articles from famous journals using a focused review question. The quality of retrieved papers was assessed through standard tools. The contents from reviewed articles were described in scientific way. Results: We included 85 papers including research and review articles and patents in this review. 18 papers introduced the theme of current review. More than 10 papers were used to describe the approaches used for synthesizing cellullose nanocomposites. Composite synthesis strategies included the in situ addition , ex situ penetration, solution mixing, and solvent casting etc. Around 60 manuscripts including 6 patents were used to demonstrate various applications of nanocellulose composites. Nanocellulose based materials offer several applications in the development of antimicrobial filters, air and water filters , filters for removal of heavy metals, pollutant sensors as well as applications in catalysis and energy sectors. Such products are more efficient, robust, reliable, and environment-friendly. Conclusion: This review gives a comprehensive picture of ongoing research and development on environmental remediation by nanotechnology. We hope that the contents reviewed herein will catch the reader's interest and will provide interesting background to extend future research activities regarding cellulose based materials.

Inflammation is considered the root cause of various inflammatory diseases, including cancers. Decursinol angelate (DA), a pyranocoumarin compound obtained from the roots of Angelica gigas, has been reported to exhibit potent anti-inflammatory effects. In this study, the anti-inflammatory effects of DA on the MAP kinase and NFκB signaling pathways and the expression of pro-inflammatory cytokines were investigated in phorbol 12-myristate 13-acetate (PMA)-activated human promyelocytic leukemia (HL-60) and lipopolysaccharide (LPS)-stimulated macrophage (Raw 264.7) cell lines. PMA induced the activation of the MAP kinase-NFκB pathway and the production of pro-inflammatory cytokines in differentiated monocytes. Treatment with DA inhibited the activation of MAP kinases and the translocation of NFκB, and decreased the expression and exogenous secretion of IL-1β and IL-6. Furthermore, LPS-stimulated Raw 264.7 cells were found to have increased expression of M1 macrophage-associated markers, such as NADPH oxidase (NOX) and inducible nitric oxide synthase (iNOS), and the M2 macrophage-associated marker CD11b. LPS also activated pro-inflammatory cytokines and Erk-NFκB. Treatment with DA suppressed LPS-induced macrophage polarization and the inflammatory response by blocking Raf-ERK and the translocation of NFκB in Raw 264.7 cells. Treatment with DA also inhibited the expression of pro-inflammatory cytokines, such as IL-1β and IL-6, NOX, and iNOS in Raw 264.7 cells. These results suggest that DA has the potential to inhibit macrophage polarization and inflammation by blocking the activation of pro-inflammatory signals. These anti-inflammatory effects of DA may contribute to its potential use as a therapeutic strategy against various inflammation-induced cancers.

Background: Most of the drugs are metabolized in the liver by the action of drug metabolizing enzymes. In hepatocellular carcinoma (HCC), primary drug metabolizing enzymes are severely dysregulated, leading to failure of chemotherapy. Sorafenib is the only standard systemic drug available, but it still presents certain limitations, and much effort is required to understand who is responsive and who is refractory to the drug. Preventive and therapeutic approaches other than systemic chemotherapy include vaccination, chemoprevention, liver transplantation, surgical resection, and locoregional therapies. Objectives: This review details the dysregulation of primary drug metabolizing enzymes and drug transport proteins of the liver in HCC and their influence on chemotherapeutic drugs. Furthermore, it emphasizes the adoption of safe alternative therapeutic strategies to chemotherapy. Conclusion: The future of HCC treatment should emphasize on understanding of resistance mechanisms and the finding of novel, safe, and efficacious therapeutic strategies, which will surely benefit patients affected by advanced HCC.

Pre-mRNA processing factor (PRPF) 4B kinase belongs to the CDK-like kinase family, and is involved in pre-mRNA splicing, and in signal transduction. In this study, we observed that PRPF overexpression decreased the intracellular levels of reactive oxygen species, and inhibited resveratrol-induced apoptosis by activating the cell survival signaling proteins NFκB, ERK, and c-MYC in HCT116 human colon cancer cells. PRPF overexpression altered cellular morphology, and rearranged the actin cytoskeleton, by regulating the activity of Rho family proteins. Moreover, it decreased the activity of RhoA, but increased the expression of Rac1. In addition, PRPF triggered the epithelial-mesenchymal transition (EMT), and decreased the invasiveness of HCT116, PC3 human prostate, and B16-F10 melanoma cells. The loss of E-cadherin, a hallmark of EMT, was observed in HCT116 cells overexpressing PRPF. Taken together, these results indicate that PRPF blocks the apoptotic effects of resveratrol by activating cell survival signaling pathways, rearranging the actin cytoskeleton, and inducing EMT. The elucidation of the mechanisms that underlie anticancer drug resistance and the anti-apoptosis effect of PRPF may provide a therapeutic basis for inhibiting tumor growth and preventing metastasis in various cancers.

Cell actin cytoskeleton is primarily modulated by Rho family proteins. RhoA regulates several downstream targets, including Rho-associated protein kinase (ROCK), LIM-Kinase (LIMK), and cofilin. Pre-mRNA processing factor 4B (PRP4) modulates the actin cytoskeleton of cancer cells via RhoA activity inhibition. In this study, we discovered that PRP4 over-expression in HCT116 colon cancer cells induces cofilin dephosphorylation by inhibiting the Rho-ROCK-LIMK-cofilin pathway. Two-dimensional gel electrophoresis, and matrix-assisted laser desorption/ionization time-of-flight mass-spectrometry (MALDI-TOF MS) analysis indicated increased expression of protein phosphatase 1A (PP1A) in PRP4-transfected HCT116 cells. The presence of PRP4 increased the expression of PP1A both at the mRNA and protein levels, which possibly activated cofilin through depho-sphorylation and subsequently modulated the cell actin cytoskeleton. Furthermore, we found that PRP4 over-expression did not induce cofilin dephosphorylation in the presence of okadaic acid, a potent phosphatase in-hibitor. Moreover, we discovered that PRP4 over-expression in HCT116 cells induced dephosphorylation of migration and invasion inhibitory protein (MIIP), and down-regulation of E-cadherin protein levels, which were further restored by the presence of okadaic acid. These findings indicate a possible molecular mechanism of PRP4-induced actin cytoskeleton remodeling and epithelial-mesenchymal transition, and make PRP4 an important target in colon cancer.

Decursinol angelate (DA), an active pyranocoumarin compound from the roots of Angelica gigas, has been
reported to possess anti-inflammatory and anti-cancer activities. In a previous study, we demonstrated
that prostaglandin E2 (PGE2) plays a survival role in HL-60 cells by protecting them from the induction of
apoptosis via oxidative stress. Flow cytometry and Hoechst staining revealed that PGE2 suppresses
menadione-induced apoptosis, cell shrinkage, and chromatin condensation, by blocking the generation of
reactive oxygen species. Treatment of DA was found to reverse the survival effect of PGE2 as well as
restoring the menadione-mediated cleavage of caspase-3, lamin B, and PARP. DA blocked PGE2-induced
activation of the EP2 receptor signaling pathway, including the activation of PKA and the phosphorylation
of CREB. DA also inhibited PGE2-induced expression of cyclooxygenase-2 and the activation of the Ras/Raf/
Erk pathway, which activates downstream targets for cell survival. Finally, DA greatly reduced the PGE2-
induced activation of NF-kB p50 and p65 subunits. These results elucidate a novel mechanism for the
regulation of cell survival and apoptosis, and open a gateway for further development and combinatory
treatments that can inhibit PGE2 in cancer cells.

The COX-2 metabolite prostaglandin E2 (PGE2) promotes inflammation and progression of several cancers, including colon
cancer. Resveratrol (3,5,4′-trihydroxy-trans-stilbene) induces apoptosis in cell lines and inhibits the invasion and metastasis
of human colon cancer. PGE2 inhibits resveratrol-induced cell death; however, the underlying mechanisms are poorly
understood. Therefore, the present study investigates the protection and survival effect of PGE2 against resveratrolinduced
apoptosis in a human colorectal carcinoma (HCT-15) cell line. HCT-15 cells were treated with resveratrol and/or
PGE2, and apoptotic cell death was assessed based on flow cytometry and the generation of reactive oxygen species
(ROS). Resveratrol reduced HCT-15 cell viability and induced cell death through the production of ROS and the
activation of caspase-3. Resveratrol treatment degraded poly (ADP-ribose) polymerase (PARP) in response to caspase-3
cleavage. Resveratrol treatment also decreased the activation of Ras-Raf-Erk and nuclear factor-κB (NF-κB) pathways
and downregulated COX-2 expression, but did not regulate the secretion of extracellular PGE2. However, PGE2 exposure
reversed resveratrol-induced oxidative stress and apoptosis, possibly through activation of the Ras-Raf-Erk pathway.
PGE2 also positively regulated NF-κB activation and markedly increased the nuclear appearance of p50 and p65
subunits. Thus, this study provides insight into the mechanisms of resveratrol-induced apoptosis. Our results suggest that
the inhibition of PGE2 and PGE2-induced activation of Ras-Raf-Erk and NF-κB signaling pathways may provide an
alternative therapeutic strategy for the treatment and prevention of colon cancer.