Multidrug-resistant (MDR) Escherichia coli ( E. coli) is a major global health threat, causing increased morbidity, mortality, and healthcare burden. It is a common cause of community- and hospital-acquired infections, with a strong ability to acquire and disseminate resistance genes via horizontal gene transfer and mutations. This review provides an overview of MDR E. coli, focusing on resistance mechanisms, diagnostic approaches, and control strategies. Key resistance mechanisms include production of extended-spectrum β-lactamases (ESBLs), carbapenemases, efflux pump overexpression, target site alterations, and reduced membrane permeability. Quorum sensing and biofilm formation further enhance bacterial survival and resistance. Diagnostic methods range from conventional antimicrobial susceptibility testing to advanced molecular and genomic techniques such as PCR and whole-genome sequencing. Emerging tools, including Fourier transform infrared spectroscopy, surface-enhanced Raman spectroscopy, MALDI-TOF MS, automated systems, and biosensors, offer rapid and accurate detection. Control strategies involve antimicrobial stewardship programs, alternative therapies such as natural compounds and QS inhibitors, and strict infection prevention measures. Addressing MDR E. coli requires a multidisciplinary approach integrating timely diagnosis, effective treatment, and robust infection control policies. A comprehensive literature search was conducted across major databases, and selected studies were qualitatively analyzed to summarize current knowledge and highlight emerging trends. Understanding these aspects is essential for limiting the spread of MDR E. coli and improving clinical outcomes globally.

Objective: To evaluate the cardioprotective effects of resveratrol and curcumin, individually and in combination, against doxorubicin-induced cardiac toxicity and explore the underlying mechanisms via network pharmacology.
Methods: In silico target prediction, enrichment analyses, and Cytoscape network modeling were performed to investigate shared molecular targets and pathways among resveratrol, curcumin and doxorubicin. Male Wistar rats (n=6/group) received oral treatments of vehicle, nebivolol (5 mg/kg), resveratrol (20 mg/kg), curcumin (100 mg/kg), resveratrol plus curcumin for 28 d, with cardiotoxicity induced via doxorubicin (2.5 mg/kg, i.p.) on days 7 and 14. Cardioprotection was evaluated using electrocardiographic, hemodynamic, biochemical, RT-PCR, and histopathological assays.
Results: Network analysis revealed four common targets (NFE2L2/Nrf2, TNF, CYP3A4, and MAPT) with significant protein-protein interaction enrichment (P=0.019 6), implicating modulation of redox balance, inflammation, and xenobiotic metabolism. Concomitant therapy with resveratrol and curcumin significantly mitigated doxorubicin-induced cardiac injury by suppressing relative heart weight, reducing myocardial infarction area, reversing electrocardiographic and conduction abnormalities, attenuating dyslipidemia, and lowering serum CK-MB, LDH, and troponin I leakage (P < 0.05). Furthermore, combination treatment was more effective in restoring cardiac antioxidants, decreasing lipid peroxidation, downregulating mRNA expressions of TNF-α and NF-κB, upregulating Nrf2 mRNA expression, and improving myocardial architecture compared with individual monotherapies.
Conclusions: Concomitant therapy with resveratrol and curcumin confers robust cardioprotection against doxorubicin-induced cardiotoxicity in rats, likely via coordinated activation of Nrf2-mediated antioxidant defenses and suppression of TNF-α/NF-κB-driven inflammation, supporting their potential for future investigation as adjunct therapies during anthracycline treatment.

Objective: To investigate the antiviral potential of Sonchus arvensis L. extracts against dengue virus (DENV)-1 and DENV-2 in vitro, and elucidate its underlying antiviral mechanisms.
Methods: The cytotoxicity of the ethanol, ethyl acetate, and n-hexane extracts of Sonchus arvensis L. was determined using the 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium assay, followed by post-treatment antiviral assays. Multiple treatment regimens were conducted to assess antiviral effects at different stages of the DENV replication cycle. qRT-PCR analysis was performed to evaluate the effects of the ethanol extract on genes associated with host innate immune and inflammatory responses.
Results: The CC₅₀ values of the ethanol, ethyl acetate, and n-hexane extracts were 391.5 μg/mL, 104.9 μg/mL, and 409.2 μg/mL, respectively. The ethanol and ethyl acetate extracts reduced DENV-1 and DENV-2 titers by >90% at 30-50 μg/mL, while the n-hexane extract showed comparable activity against DENV-2. The ethanol extract at 30 μg/mL demonstrated potent multi-stage antiviral activity, including direct virucidal, prophylactic, anti-adsorption, and anti-internalization effects. qRT-PCR analysis revealed no significant change in IFN-β expression but marked suppression of NF-κB, TNF-α, and IL-6 expression.
Conclusions: Sonchus arvensis L. ethanol extracts demonstrate potent multi-stage antiviral activity against DENV in vitro, highlighting its ability to inhibit viral entry, reduce viral replication, and attenuate excessive inflammatory responses.

Objective: To determine the qualitative and quantitative phytochemical components in the aqueous leaf extract of Trigonella foenum-graecum L. (AqE-TFG) and evaluate its therapeutic potential against high-fat diet-associated dyslipidemia in high-fat diet-induced obese rats. Methods: A total of 24 healthy adult male albino rats were randomly divided into 4 groups (n=6): Group 1 (normal control), Group 2 (untreated dyslipidemic control), Group 3 and 4 (low and high dose treatments of AqE-TFG 250 mg/kg and 500 mg/kg). Blood samples were collected for the estimation of lipid profile, oxidative markers, biochemical parameters, and histopathology of adipose tissue. Gene expression analysis was performed using qRT PCR. Results: AqE-TFG showed antioxidant activity (IC₅₀ = 4.82 µg/mL). HPLC analysis showed the presence of sinapic acid, p-coumaric acid, gallic acid, salicylic acid, kaempferol, ferulic acid, chlorogenic acid, quercetin, and HB acid. AqE-TFG remarkably inhibited body weight gain and restored the lipid profile. Furthermore, AqE-TFG elevated superoxide dismutase and catalase levels. Besides, AqE-TFG significantly downregulated mRNA expression levels of dual oxidase-related genes (Duox, Duoxa-1, Duox2) and downstream MAPK/JNK signaling cascade genes (MAPK8, Traf4, Traf6). Adipose tissue histology showed well-organized, intact adipocytes in treatment groups. Conclusions: AqE-TFG has both preventive and therapeutic effects against high-fat diet-induced dyslipidemia. AqE-TFG could enhance antioxidant defense and restore histopathological lesions via MAPK/JNK signaling pathway.