Neem extract-blended nanocellulose derived from jackfruit peel for antibacterial packagings.

The use of jackfruit peel as a source for natural and fully biodegradable "nanocellulose" (NC) for the production of bioplastics with Azadirachta indica (A. indica) extracts and polyethylene glycol (PEG) for the antibacterial properties is investigated. The characterization of the biocomposite using FT-IR and WXRD was reported. The physicochemical properties including thickness, moisture content, water holding capacity, swelling, porosity, and biodegradability in soil were investigated. The incorporation of A. indica extract revealed an increased shelf life due to the strong antibacterial activity, and these biocomposites were degraded in soil within 60 days after the end use without any harm to the environment. Jackfruit-derived nanocellulose film blended with A. indica extract exhibited strong antibacterial activity against gram-positive and gram-negative food spoilage bacteria. Disc diffusion assay, live/dead assay, and CFU analysis confirmed the antibacterial property of the synthesized film. Moreover, the films clearly prevented the biofilm formation in bacteria. Thus, the developed bioplastics can be utilized as appropriate substitutes to food packaging materials and also for biomedical applications such as wound dressings.

Integrated biorefinery development for pomegranate peel: Prospects for the production of fuel, chemicals and bioactive molecules.

Current experimental evidence has revealed that pomegranate peel is a significant source of essential bio compounds, and many of them can be transformed into valorized products. Pomegranate peel can also be used as feedstock to produce fuels and biochemicals. We herein review this pomegranate peel conversion technology and the prospective valorized product that can be synthesized from this frequently disposed fruit waste. The review also discusses its usage as a carbon substrate to synthesize bioactive compounds like phenolics, flavonoids and its use in enzyme biosynthesis. Based on reported experimental evidence, it is apparent that pomegranate peel has a large number of applications, and therefore, the development of an integrated biorefinery concept to use pomegranate peel will aid in effectively utilizing its significant advantages. The biorefinery method displays a promising approach for efficiently using pomegranate peel; nevertheless, further studies should be needed in this area.

Musa paradisiaca inflorescence induces human colon cancer cell death by modulating cascades of transcriptional events.

Colorectal cancer (CRC) is one of the leading causes of cancer death, and diet plays an important role in the etiology of CRC. Traditional medical practitioners in many South Asian countries use plantain inflorescence to treat various gastro-intestinal ailments. The aim of the present study was to investigate the anticancer effects of extracts of inflorescence of Musa paradisiaca against HT29 human colon cancer cells and elucidate the mechanism of these effects by studying the modulation of cascades of transcriptional events. In vitro assays depicted that methanol extract of Musa paradisiaca inflorescence (PIMET) was cytotoxic to HT29 cells. PIMET induced DNA damage and arrested the cell cycle at the G2/M phase. Expression studies showed that PIMET pretreatment upregulates pro-apoptotic Bcl2 and downregulates anti-apoptotic Bax proteins. Different assays showed that the deregulation of pro/antiapoptotic proteins reduces the mitochondrial membrane potential and ATP production; moreover, it enhances cytochrome c release, which triggers the apoptotic pathway, and further cleaves caspase 3 and PARP proteins, resulting in apoptosis. Changes in the protein expression profile of HT29 cells after PIMET treatment were analyzed using mass-spectrometry-based proteomics. PIMET treatment significantly altered the expression of HT29 protein; interestingly, X-linked inhibitor of apoptosis protein was also downregulated. Alteration in the expression of this protein has significant effects, leading to HT29 cell death.