Green Synthesis of Metal and Metal Oxide Nanoparticles Using Different Plants’ Parts for Antimicrobial Activity and Anticancer Activity: A Review Article

Nanotechnology emerged as a scientific innovation in the 21st century. Metallic nanoparticles (metal or metal oxide nanoparticles) have attained remarkable popularity due to their interesting biological, physical, chemical, magnetic, and optical properties. Metal-based nanoparticles can be prepared by utilizing different biological, physical, and chemical methods. The biological method is preferred as it provides a green, simple, facile, ecofriendly, rapid, and cost-effective route for the green synthesis of nanoparticles. Plants have complex phytochemical constituents such as carbohydrates, amino acids, phenolics, flavonoids, terpenoids, and proteins, which can behave as reducing and stabilizing agents. However, the mechanism of green synthesis by using plants is still highly debatable. In this report, we summarized basic principles or mechanisms of green synthesis especially for metal or metal oxide (i.e., ZnO, Au, Ag, and TiO2, Fe, Fe2O3, Cu, CuO, Co) nanoparticles. Finally, we explored the medical applications of plant-based nanoparticles in terms of antibacterial, antifungal, and anticancer activity

Comparative Effect of Seed Coating and Biopriming of <i>Bacillus aryabhattai</i> Z-48 on Seedling Growth, Growth Promotion, and Suppression of Fusarium Wilt Disease of Tomato Plants

Beneficial plant microbes can enhance the growth and quality of field crops. However, the benefits of microbes using cheap and efficient inoculation methods are still uncommon. Seed coating with biocontrol agents can reduce the amount of inocula along with having the potential for large-scale application. Hence, in this research work, the comparative potential of tomato seed coating and biopriming with Bacillus aryabhattai Z-48, harboring multiple plant-beneficial traits, to suppress Fusarium wilt disease along with its beneficial effect on seedling and plant growth promotion was analyzed. Among two bacterial strains, B. aryabhattai Z-48 was able to antagonize the mycelial growth of Fusarium oxysporum f.sp. lycopersici in vitro and its application as a seed coating superiorly benefited seedling traits like the germination percentage, vigor index, and seedling growth index along with a reduced germination time. The seed coating with B. aryabhattai Z-48 resulted in significant increases in the shoot length, root length, dry biomass, and total chlorophyll contents when compared with the bioprimed seeds with the same bacterial strain and non-inoculated control plants. The seed coating with B. aryabhattai Z-48 significantly reduced the disease index (>60%) compared with the pathogen control during pot trials. Additionally, the seed coating with B. aryabhattai Z-48 resulted in a significantly higher production of total phenolics, peroxidase, polyphenol oxidase, and phenylalanine ammonia lyase enzyme in tomato plants. The GC/MS-based non-targeted metabolic profiling indicated that the seed coating with B. aryabhattai Z-48 could cause large-scale metabolite perturbations in sugars, sugar alcohols, amino acids, and organic acids to increase the fitness of tomato plants against biotic stress. Our study indicates that a tomato seed coating with B. aryabhattai Z-48 can improve tomato growth and suppress Fusarium wilt disease effectively under conventional agricultural systems

Cucurbitacin E reduces obesity and related metabolic dysfunction in mice by targeting JAK-STAT5 signaling pathway

<div><p>Several members of cucurbitaceae family have been reported to regulate growth of cancer by interfering with STAT3 signaling. In the present study, we investigated the unique role and molecular mechanism of cucurbitacins (Cucs) in reducing symptoms of metabolic syndrome in mice. Cucurbitacin E (CuE) was found to reduce adipogenesis in murine adipocytes. CuE treatment diminished hypertrophy of adipocytes, visceral obesity and lipogenesis gene expression in diet induced mice model of metabolic syndrome (MetS). CuE also ameliorated adipose tissue dysfunction by reducing hyperleptinemia and TNF-alpha levels and enhancing hypoadiponectinemia. Results show that CuE mediated these effects by attenuating Jenus kinase- Signal transducer and activator of transcription 5 (JAK- STAT5) signaling in visceral fat tissue. As a result, CuE treatment also reduced PPAR gamma expression. Glucose uptake enhanced in adipocytes after stimulation with CuE and insulin resistance diminished in mice treated with CuE, as reflected by reduced glucose intolerance and glucose stimulated insulin secretion. CuE restored insulin sensitivity indirectly by inhibiting JAK phosphorylation and improving AMPK activity. Consequently, insulin signaling was up-regulated in mice muscle. As CuE positively regulated adipose tissue function and suppressed visceral obesity, dyslipedemia, hyperglycemia and insulin resistance in mice model of MetS, we suggest that CuE can be used as novel approach to treat metabolic diseases.</p></div

Determination of the effect of CuE on insulin signaling.

<p>(A) Total protein from skeletal muscle of all mice groups was separated on 7.5% SDS-PAGE gels, and immunoblotted with either phospho IRS-1 serine 307 or phospho AKT serine 473 or phospho-AMPK-Thr 172 or phospho JAK-tyrosine1007/1008 antibody. (B) The levels of phosphorylation in the immunoblots were quantified using densitometry and normalized to their respective total proteins expression. The data are presented as mean ± SEMs, n = 5–6, *P < 0.05 mice treated with CuE or Orlistat vs HFD-MetS mice.</p

Structure of cucurbitacins.

<p>Structure of cucurbitacins.</p

Effect of cucurbitacins on adipogenesis.

<p>(A) Oil red O staining in 3T3-L1 preadipocytes differentiated into adipocytes and treated with different concentrations of cucurbitacins. GM, growth media, DM, differentiation media. (B) Quantification of cellular TG content. Cellular triglyceride content is relative to cells treated with DM alone (deemed 100%). n = 4–5 independent experiments, results represent mean ± SEMs. *P < 0.05, cucurbitacins vs. cells treated with DM alone. (C) Glucose uptake in adipocytes. Differentiated 3T3-L1 adipocytes were incubated with 20ng/ml TNF-alpha and CuE for 24 hours followed by stimulation with 10nM insulin for 1 hour. Results are mean ± SEMs of five experiments, *P < 0.05. cucurbitacins vs. cells treated with TNF-alpha alone.</p

Determination of the effect of CuE on JAK-STAT signaling.

<p>(A) Total protein from abdominal fat of all mice groups was separated on 7.5% SDS-PAGE gels, and immunoblotted with a phospho-tyrosine1007/1008 antibody. The same blots were stripped and reprobed with a polyclonal JAK-2 protein antibody. The levels of tyrosine phosphorylation of JAK-2 in the immunoblots were quantified using densitometry and normalized to the JAK-2 protein. (B) Phospho STAT5A tyrosine 694 antibody was used for immunoblotting STAT5A phosphorylation. (C) PPAR-gamma antibody was used to measure expression of PPAR-gamma. The data are presented as mean ± SEMs, n = 5–6, *P < 0.05 mice treated with CuE or Orlistat vs HFD-MetS mice.</p

Effect of CuE on adipose tissue morphology and function.

<p>(A) H and E stained tissue of perigonadal fat from (I) SD (II) HFD (III) HFD+CuE (L) (IV) HFD+CuE (H); and (V) HFD+Orlistat mice. (B-D) Lipogenic gene expression of SREBP, FASN and ACACA genes was measured in visceral fat tissue, by quantitative PCR. (E) Serum adiponectin concentration. (F) Serum leptin levels were measured by ELISA. (G-I) Macrophage infiltration and recruitment gene expression of CD11b, MCP-1 and CCR2 genes was measured in visceral fat tissue, by quantitative PCR. *P < 0.05 HFD-MetS mice treated with CuE or Orlistat vs HFD mice model of MetS. Results are mean ± S.E. (n = 12–15). (J) Serum TNF-alpha concentration.</p

CuE treatment improved insulin resistance in mice.

<p>(A) Measurement of blood glucose levels in mice when challenged with intraperitoneal glucose tolerance test (IP-GTT). Area under the curve (AUC) quantification for GTT. (B) Measurement of blood insulin levels during IP-GTT. Area under the curve (AUC) quantification for glucose stimulated insulin secretion (GSIS). Results represent mean ± SEMs. n = 10–12 in each group, *P < 0.05, mice treated with CuE or Orlistat vs HFD mice model of MetS.</p