Hepatocellular carcinoma (HCC) is the predominant type of primary liver cancer, with a rising global incidence and a high mortality rate. Chronic infections with hepatitis viruses, along with risk factors such as cirrhosis, metabolic dysfunction-associated steatohepatitis, and metabolic disorders, significantly contribute to HCC development. Systemic inflammation plays a key role in HCC pathogenesis, with inflammatory markers such as the neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) emerging as significant prognostic indicators. Elevated NLR and PLR are associated with poor overall survival and progression-free survival in HCC patients, reflecting an imbalance in the immune response and tumor microenvironment (TME). Neutrophils and platelets contribute to tumor progression by promoting inflammation, angiogenesis, and immune evasion, while lymphocytes, particularly CD8+ T-cells, play essential roles in antitumor immunity. High levels of NLR and PLR are linked to adverse clinical outcomes, including shorter survival times and higher recurrence rates. These ratios provide valuable prognostic information and are increasingly utilized in clinical settings to guide treatment decisions. This review focuses on the roles of inflammatory markers, particularly NLR and PLR, in HCC progression and prognosis, examining their effects on the TME and their potential for improving diagnostic and prognostic strategies. The use of these inflammatory markers and emerging technologies holds promise for enhancing early detection and personalized treatment strategies, ultimately improving patient outcomes in HCC.

Hepatocellular carcinoma (HCC) is the fifth most common and fatal cancer reported, representing 72.5% of malignancies around the world. The majority of HCC incidents have been associated with infections caused by hepatitis B and C viruses. Many first- and second-line conventional drugs, e.g., sorafenib, cabozantinib, or ramucirumab, have been used for the management of HCC. Despite different combinational therapies, there are still no defined biomarkers for an early stage diagnosis of HCC. The current study evaluated the potential of Bergenia stracheyi, Bergenia ciliata, Bergenia pacumbis, and Bergenia purpurascens, which belong to the family Saxifragaceae, to treat HCC using an integrated network pharmacology and molecular docking approach. Four active phytochemicals were selected based on oral bioavailability (OB) and drug likeness (DL) parameters. The criteria of phytochemical selection were set to OB > 30% and DL > 0.18. Similarly, the gene targets related to Bergenia spp. and the genes related to HCC were retrieved from different databases. The integration of these genes revealed 98 most common overlapping genes, which were mainly interrelated with HCC pathogenesis. Ultimately, the 98 Bergenia-HCC associated genes were used for protein–protein interaction (PPI), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway, and Gene Ontology (GO) enrichment analyses. Finally, the topological analysis revealed the top ten hub genes with maximum degree rank. From the top ten genes, STAT3, MAPK3, and SRC were selected due to their involvement in GO annotation and KEGG pathway. To confirm the network pharmacology results, molecular docking analysis was performed to target STAT3, MAPK3, and SRC receptor proteins. The phytochemical (+)-catechin 3-gallate exhibited a maximum binding score and strong residue interactions with the active amino acids of MAPK3-binding pockets (S-score: −10.2 kcal/mol), SRC (S-score: −8.9 kcal/mol), and STAT3 (S-score: −8.9 kcal/mol) as receptor proteins. (+)-Catechin 3-gallate and β-sitosterol induced a significant reduction in cell viability in HepG2 after 24 h of treatment in a dose-dependent manner. The results of this study explore the potential of (+)-catechin 3-gallate and β-sitosterol, which can be used in the future as potential drug candidates to suppress HCC.

The study of the TLR (Toll-like receptor) family has progressed our knowledge of the intrinsic insusceptible framework. The familiar resistant of microorganisms' constitutive and protected substances is the reason for intrinsic insusceptible response. Similarly, TLRs can be blocked by damaging substances. Favorable to provocative cytokines are created when TLRs are actuated by microbial or have determined mixtures that can be valuable or unsafe to the host. TLRs are found in an assortment of organs, including those of the cardiovascular framework, notwithstanding invulnerable cells. This review takes a gander at the job of TLRs in septic cardiomyopathy, viral myocarditis, there is a lack of knowledge not only about the role of clear to the TLRs in starting and coordinating homoeostatic processes inside the heart, but also about stressed actuated TLR enactment in cardiovascular framework tissues. As per mounting proof, TLRs might assume a part in the pathogenesis of atherosclerosis, viral myocarditis, widened cardiomyopathy, heart allograft dismissal, and sepsis-actuated left ventricular brokenness.