Phytochemical analysis, in vitro antioxidant and antimicrobial activities of male flower of Juglans regia L.

The male flower of Juglans regia L., were investigated for its in vitro antioxidant activity, antimicrobial activity, and chemical constituents. The antioxidant activity showed that the methanol extract of J. regia male flower (MEJR) had highest scavenging potential than the other solvents (ethanolic = EEJR and aqueous = AEJR). The antimicrobial activity showed that Staphylococcus aureus and Escherichia coli were the most sensitive organisms and significant activity was also recorded against both the fungal strains tested, with highest activity against Candida albicans. Totally, 26 constituents were identified by high-resolution-liquid chromatography-mass spectrometry analyses from which seven compounds were identified first time from the extract

Juglans regia L. protects against UVB induced apoptosis in human epidermal keratinocytes

The present study was aimed to investigate the photoprotective effect of the male flower of J. regia L. (MEJR) against ultraviolet-B induced apoptosis in human skin cells. Human skin epidermal keratinocytes were pretreated with the MEJR (80 µg/ml, has been selected after MTT assay), prior to 30 min UVB-irradiation at a dose of 20 mJ/cm2. Mitochondrial membrane potential was evaluated using Rhodamine-123 staining; the % apoptosis by Hoechst staining and acridine orange staining; DNA damage was measured by comet assay. The levels of p53, Bax, Bcl-xL, Bcl-2, Cytochrome c, Caspase-9 and Caspase-3 expression in HaCaT cells were analyzed by western blotting and RT-PCR. Pretreatment with MEJR 80 µg/ml prior to UVB-irradiation significantly prevents apoptotic characteristics, DNA damage and loss of mitochondrial membrane potential. Thus, MEJR protects UVB-mediated human skin cells, by modulating the expression of apoptotic markers and UVB-induced DNA damage in HaCaT cells. Keywords: Juglans regia L., Ultraviolet-B, DNA damage, Apoptotic marker

Phytochemicals as modulators of ultraviolet-b radiation induced cellular and molecular events: A review

Ultraviolet (UV) radiation is a very prominent environmental toxic agent. Particularly, UVB (280–320 nm – short wave) wavelength penetrates the epidermis and is completely absorbed in the upper dermis, whereas UVA (320–400 nm - long wave) penetrates to the deeper dermis. UVA is a relatively weak carcinogen than UVB because of its weak strength as a tumor initiating agent. UVB exposure elicits adverse effect which includes sunburn, basal and squamous cell carcinoma, melanoma, cataracts, photoaging of the skin and immunosuppression. Increased ozone depletion and modern lifestyle has increased the amount of UV exposure, and this consequently led to a surge in the incidence of skin cancer. UVB-irradiation acts as both tumor initiator and tumor promoter in animal models. UVB-initiated signal transduction pathways are believed to be responsible for tumor promotion effects. Variety of cellular changes, which includes activation of transcription factors and protein kinases were altered during acute and chronic UVB-exposure. All these events leads to skin cancer development involving DNA damage, inflammation, immunosuppression, epidermal hyperplasia, cell cycle dysregulation, depletion of antioxidant–defenses, and reactive oxygen species generation. An epidemiological study shows that human beings consuming varieties of vegetables and fruits are protected from UVB induced carcinogenesis. In the recent years, number of experimental evidences showed that natural nutraceuticals and phytoceuticals are vital targets for UVB-mediated cellular and molecular events and prevents cellular milieu from UVB mediated health effects. In this review, we have discussed the current progress in the study on UVB-mediated signaling that can be exploited as targets for phytochemicals

Potential role of probiotic species in ameliorating oxidative stress, effect on liver profile and hormones in male albino rat model

Probiotics are living micro-organism preparations which can vigorously inhibit the probable pathogens colonization in the gut microbial ecology. Current experiment was designed to investigate the efficacy of imported probiotic species compared with the indigenous probiotics species on the oxidative stress, enzymes, and hormones in animal model. Thirty Albino rats were equally divided into three groups with 10 rats ( n  = 10) in each group as Control (C), supplemented with imported probiotic species (IP), and supplemented with indigenous probiotics species (InP) for 21 days under controlled environment. The evaluation of treatments was done by testing the serum oxidative stress markers, liver enzymes (Aspartate transaminase and Alanine aminotransferase), lipid profile, and hormonal dynamics including Lutinizing hormone (LH), follicular stimulating hormone (FSH), and growth hormone (GH) in albino male rats. Results revealed that use of indigenous probiotic species significantly ( p  < 0.05) reduces the oxidative stress and improves the antioxidant capacity; liver enzymes, total cholesterol, and LDL-Cholesterol were also reduced significantly ( p  < 0.05) in InP as compared to IP group. Moreover, results of hormones including LH, FSH, and GH explored that indigenous probiotics have significant ( p  < 0.05) potential to improve these hormones as compared to imported probiotics. Although, it could be concluded that InP have beneficial role in preventing the body from oxidative stress as well as in improving the blood parameters but comprehensive studies are required to investigate the detail gut ecology of the indigenous species which will definitely a strong support in preparing a more suitable local probiotic supplement

Insight into Oncogenic Viral Pathways as Drivers of Viral Cancers: Implication for Effective Therapy

As per a recent study conducted by the WHO, 15.4% of all cancers are caused by infectious agents of various categories, and more than 10% of them are attributed to viruses. The emergence of COVID-19 has once again diverted the scientific community’s attention toward viral diseases. Some researchers have postulated that SARS-CoV-2 will add its name to the growing list of oncogenic viruses in the long run. However, owing to the complexities in carcinogenesis of viral origin, researchers across the world are struggling to identify the common thread that runs across different oncogenic viruses. Classical pathways of viral oncogenesis have identified oncogenic mediators in oncogenic viruses, but these mediators have been reported to act on diverse cellular and multiple omics pathways. In addition to viral mediators of carcinogenesis, researchers have identified various host factors responsible for viral carcinogenesis. Henceforth owing to viral and host complexities in viral carcinogenesis, a singular mechanistic pathway remains yet to be established; hence there is an urgent need to integrate concepts from system biology, cancer microenvironment, evolutionary perspective, and thermodynamics to understand the role of viruses as drivers of cancer. In the present manuscript, we provide a holistic view of the pathogenic pathways involved in viral oncogenesis with special emphasis on alteration in the tumor microenvironment, genomic alteration, biological entropy, evolutionary selection, and host determinants involved in the pathogenesis of viral tumor genesis. These concepts can provide important insight into viral cancers, which can have an important implication for developing novel, effective, and personalized therapeutic options for treating viral cancers