Citronellol (CT) is a naturally occurring lipophilic monoterpenoid which has shown anticancer effects in numerous cancerous cell lines. This study was, therefore, designed to examine CT's potential as an anticancer agent against glioblastoma (GBM). Network pharmacology analysis was employed to identify potential anticancer targets of CT. A comprehensive data mining was carried out to assess CT and GBM‐associated target genes. Protein–protein interaction network was constructed to identify hub genes and later GO and KEGG enrichment analysis was performed to elucidate the possible mechanism. Human glioblastoma cell line “SF767” was used to confirm in silico findings. MTT, crystal violet, and trypan blue assays were performed to assess the cytotoxic effects of various concentrations of CT. Subsequently, ELISA and qPCR were performed to analyze the effects of CT on proapoptotic and inflammatory mediators. In silico findings indicated that CT differentially regulated proapoptotic and inflammatory pathways by activating caspase‐3 and 8 and inhibiting nuclear factor‐kappa B (NF‐κB), tumor necrosis factor‐α, Janus kinase 2 (JAK2). Molecular docking also demonstrated strong binding affinities of CT with the above‐mentioned mediators when compared to 5‐fluorouracil or temozolomide. In SF767 cell line, CT displayed dose‐dependent cytotoxic and antioxidant effects, and upregulation of annexin‐V, caspase‐3, and 8 along with downregulation of inflammatory modulators. In a nutshell, it can be concluded from these findings that CT possesses robust anticancer activity which is mediated via differential regulation of caspase‐3, JAK2, and NF‐κB pathways.

Background: This study aimed to evaluate the anti-inflammatory effects of a Zephyranthes rosea in an ovalbumin-induced asthma model. Methods: Allergic asthma was induced in mice via intraperitoneal injection, followed by intranasal ovalbumin challenge. Methanolic extract of Z. rosea bulb was orally administered to asthmatic mice for 14 days. Hematological parameters for bronchoalveolar lavage fluid (BALF) and blood were analyzed. The mRNA expression levels of interleukins and transforming growth factor beta (TGF-β1) in lung tissues were determined using reverse transcriptase–polymerase chain reaction (RT–PCR). Network pharmacology analysis was used to find possible Z. rosea targets. After building a protein–protein interaction network to find hub genes, GO and KEGG enrichment analyses were carried out to determine the potential mechanism. In silico analysis was performed by Molecular Operating Environment. Results: GC-MS analysis of Z. rosea extract detected major classes of phytochemicals. Hematological parameters in blood and BALF from Z. rosea extract-treated animals were significantly reduced in a dose-dependent fashion. Histopathology revealed that Z. rosea bulb had an ameliorative effect on lung tissues. Moreover, treatment with Z. rosea bulb extract significantly restored the normal levels of IL-4, IL-6, IL-1β, IL-10, IL-13, and TGF-β1 in allergic asthmatic mice compared to the diseased group. In silico analysis, particularly of the binding affinities of Z. rosea bulb phytoconstituents for IL6, AKT1, and Src, supported in vivo results. Conclusions: These findings indicated that Z. rosea bulb extract significantly ameliorates cellular and molecular biomarkers of bronchial inflammation and could be a potential candidate for treating allergic asthma.

Rheumatoid arthritis (RA) is a chronic inflammatory condition that affects millions of people globally, often leading to morbidity. Recent research highlights the potential of natural products in managing arthritis symptoms and modifying disease progression. Among these, Melaleuca alternifolia oil (MAO) has emerged as a promising therapeutic option due to its anti‐inflammatory and analgesic properties. A total of 36 Sprague–Dawley rats weighing between 200 and 220 g were divided into six groups ( n = 6). On day 0, arthritis was induced by CFA. On day 8, treatment started and lasted till day 28. Paw edema and arthritic score were measured. Moreover, hematological, histological, and biochemical parameters were evaluated. The mRNA expression levels of anti‐inflammatory cytokine IL‐4 and pro‐inflammatory cytokines such as TNF‐α, IL‐6, NF‐κB, and IL‐1β were measured using real‐time polymerase chain reaction (qPCR). ELISA was used to detect PGE2 levels. Network pharmacology was used to evaluate the hub genes between the phytocompounds and rheumatoid arthritis. Molecular docking and scoring calculations were done for the top matched hub genes for moderate confirmations between phytocompounds and targets. GC–MS analysis was also performed to identify potential anti‐inflammatory constituents present in the plant oil. Treatment with MAO effectively reduced paw edema and swelling. Histopathological examinations demonstrated significant improvement in the treatment groups. Biochemical parameters such as creatinine, urea, alanine aminotransferase (ALT), and alkaline phosphatase (ALP) did not significantly alter, and hematological parameters such as red blood cells (RBC), white blood cells (WBC), hemoglobin (Hb), and platelet count were restored in the treated group. The mRNA expression of anti‐inflammatory cytokines, including IL‐4, was upregulated, and pro‐inflammatory biomarkers such as TNF‐α, IL‐1β, IL‐6, and NF‐κB were significantly downregulated in the arthritic control group. Furthermore, treatment with MAO significantly reduced PGE2 levels. Network pharmacology indicated the hub genes and several biological processes, molecular functions, cellular components, and KEGG pathways that are involved in rheumatoid arthritis. Molecular docking was performed against hub genes such as AKT1, BCL‐2, MAPK3, and MMP9 that are involved in various pro‐inflammatory cytokine formation and pathophysiology of rheumatoid arthritis. GC–MS analysis of the plant's oil revealed the presence of numerous anti‐inflammatory and antirheumatic phytochemicals. MAO possesses considerable anti‐arthritic properties by downregulating pro‐inflammatory biomarkers such as IL‐1β, NF‐κB, IL‐6, TNF‐α, and upregulating anti‐inflammatory IL‐4. Further investigations are needed to explore its potential as a natural therapeutic option for treating RA.