Ranunculus arvensis L. (R. arvensis) has long been used to treat a variety of medical conditions such as arthritis, asthma, hay fever, rheumatism, psoriasis, gut diseases and rheumatic pain. Here, we screened R. arvensis for antioxidant activity, phytochemical and high performance liquid chromatography (HPLC) analyses. The chloroform, chloroform:methanol, methanol, methanol:acetone, acetone, methanol:water and water extracts of R. arvensis were examined for DPPH (1, 1-diphenyl-2-picrylhydrazyl) free radical scavenging assay, hydrogen peroxide scavenging assay, phosphomolybdenum assay, reducing power assay, flavonoid content, phenolic content and high performance liquid chromatography analysis. Significant antioxidant activity was displayed by methanol extract (IC 50 34.71 ± 0.02) in DPPH free radical scavenging assay. Total flavonoids and phenolics ranged 0.96–6.0 mg/g of extract calculated as rutin equivalent and 0.48–1.43 mg/g of extract calculated as gallic acid equivalent respectively. Significant value of rutin and caffeic acid was observed via high performance liquid chromatography. These results showed that extracts of R. arvensis exhibited significant antioxidant activities. Moreover, R. arvensis is a rich source of rutin, flavonoids and phenolics.

Different physical and chemical techniques are used for the decontamination of Cr⁺⁶ contaminated sites. The techniques are expensive, laborious, and time-consuming. However, remediation of Cr⁺⁶ by microbes is viable, efficient, and cost-effective. In this context, plant growth-promoting rhizobacteria Acinetobacter bouvetii P1 isolated from the industrial zone was tested for its role in relieving Cr⁺⁶ induced oxidative stress in sunflower. At the elevated Cr⁺⁶ levels and in the absence of P1, the growth of the sunflower plants was inhibited. In contrast, the selected strain P1 restored the sunflower growth under Cr⁺⁶ through plant growth–promoting interactions. Specifically, P1 biotransformed the Cr⁺⁶ into a stable and less toxic Cr⁺³ form, thus avoiding the possibility of phytotoxicity. On the one hand, the P1 strengthened the host antioxidant system by triggering higher production of enzymatic antioxidants, including catalases, ascorbate peroxidase, superoxide dismutase, and peroxidase. Similarly, P1 also promoted higher production of nonenzymatic antioxidants, such as flavonoids, phenolics, proline, and glutathione. Apart from the bioremediation, P1 solubilized phosphate and produced indole acetic acid, gibberellic acid, and salicylic acid. The production of phytohormones not only helped the host plant growth but also mitigated the harsh condition posed by the elevated levels of Cr⁺⁶. The findings mentioned above suggest that P1 may serve as an excellent phyto-stimulant and bio-remediator in a heavy metal-contaminated environment.

Metastasis, which is controlled by concerted action of multiple genes, is a complex process, and is important cause of cancer death. KLF17 is a negative regulator of metastasis and epithelial-mesenchymal-transition (EMT) during cancer progression. However, the underlying molecular mechanism and biological relevance of KLF17 in cancer cells are poorly understood. Here, we show that tumor suppressor protein p53 plays an integral role to induce KLF17 expression in NSCLC. p53 is recruited to KLF17 promoter and results in the formation of p53-DNA complex. p53 enhances binding of p300, and favors histone acetylation on KLF17 promoter. Mechanistically, p53 physically interacts with KLF17 and thereby enhances anti-metastatic function of KLF17. p53 empowers KLF17 mediated EMT genes transcription via enhancing physical association of KLF17 to target gene promoters. Nutlin-3 recruits KLF17 to EMT target gene promoters and results in the formation of KLF17-DNA complex via p53-dependent pathway. p53 depletion abrogates DNA binding affinity of KLF17 to EMT target gene promoters. KLF17 is critical for p53 cellular activities in NSCLC. Importantly, KLF17 enhances p53 transcription to generate a novel positive feedback loop. KLF17 depletion accelerates lungs cancer cells growth in response to chemotherapy. Mechanistically, we found that KLF17 increases tumor suppressor genes p53, p21 and pRB expressions in NSCLC. Functionally, KLF17 required p53 to suppress cancer cell invasion and migration in NSCLC. In sum, our study highlights novel insight into anti-EMT affect of KLF17 via p53-dependent pathway in NSCLC, and KLF17 may be a new therapeutic target in NSCLC with p53 status.

The clinical outcomes of patients infected with hepatitis C virus (HCV) range from acute resolving hepatitis to chronic liver diseases such as liver cirrhosis or hepatocellular carcinoma. Identification of the infecting virus genotype is indispensable for the exploration of many aspects of HCV infection, including epidemiology, pathogenesis, and response to antiviral therapy. 1419 individuals were screened for anti-HCV in this study, of which 166 (11.7%) were found reactive by ICT (Immunochromatographic test). These 166 anti-HCV positive and 26 normal individuals were further analyzed. RNA was extracted from serum and reverse-transcribed to cDNA and the core region of HCV genome was targeted and amplified by multiplex PCR. HCV RNA was detected in 121 individuals, of which 87 were male and 34 were female. Genotype 3a was the most prevalent among all the genotypes observed followed by 3b. Genotypes 1a, 2a, and 2b were found in 10.89%, 13.22%, and 6.61% patients, respectively. 25.41% of the HCV RNA positive samples were not typed. 6.05% of patients were found having mixed genotypes. These findings will not only help the physicians to prescribe more appropriate treatment for the HCV infection but will also draw the attention of health-related policy makers to devise strategies to curb the disease more effectively.

Inflammation coupled with oxidative stress contribute to the pathogenicity of various clinical disorders. Oxidative stress arises from an imbalance between production of reactive oxygen species (ROS) and antioxidant defense system, leading to cellular damages. The study investigated the antioxidant and anti-inflammatory effects of polysaccharides isolated from Lepidium sativum seed-coat mucilage. The water-soluble polysaccharides were extracted from mucilage and fractionated using gel permeation chromatography. The radical scavenging potential of various fractions was determined using DPPH, H₂O₂, and lipid peroxidation assays. The most effective EC₅₀ was recorded for F53 (57.41 ± 1.34 μg/mL), followed by F20 (69.19 ± 0.61 μg/mL) and F52 (75.06 ± 0.45 μg/mL). In vitro anti-inflammatory effect was determined through human membrane stabilization assay while the in vivo effect was evaluated using a carrageenan-induced paw edema in mouse model where F53 demonstrated significant (P = 0.05) anti-inflammatory potential (92.60 % compared to diclofenac sodium 91.46 %). GC-MS analysis revealed the presence of galacturonic acid and glucuronic acid as main acidic monosaccharides along with varying quantities of rhamnose, arabinose, and maltose as prominent neutral monosaccharides. The study concludes that cress seed mucilage contains potent antioxidant and anti-inflammatory polysaccharides. Further studies on the mode of action of these polysaccharides could provide deeper insights into their potential use as antioxidant and anti-inflammatory agents.