Smart self-healing coatings offer a revolutionary approach to mitigating metal corrosion, a problem with significant economic and environmental impacts. Divided into intrinsic and extrinsic types, these coatings autonomously rectify the damage. Intrinsic variants utilize reversible bonds to achieve ongoing repair, while extrinsic ones incorporate micro/nanocontainers that activate upon environmental triggers to mend micro-cracks, their efficacy dictated by the encapsulated healing agents’ volume. This review dissects the rapidly evolving sector of stimuli-responsive self-healing coatings, emphasizing the progress in micro/nano container technology. It discusses the synthesis and encapsulation processes of different micro/nanocontainers and charts the transition from single to multistimulus-responsive systems, which enhances the coatings’ sensitivity and functionality. The addition of multifunctional traits such as self-reporting and anti-microbial actions further broadens their industrial applicability. The review provides a succinct overview of the field’s current state and future potential, envisioning a paradigm shift in corrosion protection through advanced smart coatings.

In this study, the methanolic extract from seeds of Gardenia jasminoides exhibited strong antioxidant and enzyme inhibition activities with less toxicity to NIH3T3 and HepG2 cells at the concentration of 100 µg/mL. The antioxidant activities (DPPH and ABTS), α-amylase, and α-glucosidase inhibition activities were found higher in methanolic extract (MeOH-E) than H₂O extract. Besides, 9.82 ± 0.62 µg and 6.42 ± 0.26 µg of MeOH-E were equivalent to 1 µg ascorbic acid for ABTS and DPPH scavenging, respectively while 9.02 ± 0.25 µg and 6.52 ± 0.15 µg of MeOH-E were equivalent to 1 µg of acarbose for inhibition of α-amylase and α-glucosidase respectively. Moreover, the cell assay revealed that the addition of MeOH-E (12.5 µg/mL) increased about 37% of glucose uptake in insulin resistant (IR) HepG2 as compared to untreated IR HepG2 cells. The LC- MS/MS and GC-MS analysis of MeOH-E revealed a total of 54 compounds including terpenoids, glycosides, fatty acid, phenolic acid derivatives. Among the identified compounds, chlorogenic acid and jasminoside A were found promising for anti-diabetic activity revealed by molecular docking study and these molecules are deserving further purification and molecular analysis.

Traditional, complementary, and integrative medicine are globally accepted alternative methods for the treatment of diabetes mellitus (DM). However, the mechanism of anti-diabetic effects of Helianthus tuberosus L. remains unproven. In the present study, antioxidant and anti-diabetic activity of the tubers of H. tuberosus were studied in detail. Methanolic extracts of H. tuberosus tubers were subjected to solvent fractionation method by increasing the polarity of the solvent using n-hexane, and ethyl acetate. The obtained methanol extracts and its fractions were subjected to free radical scavenging activity (DPPH and ABTS assay) and in vitro enzyme (α-amylase and α-glucosidase) inhibition assay. Moreover, glucose uptake in insulin-resistant HepG2 cell line was analyzed. The preliminary phytochemical analysis confirmed the presence of phenolic and flavonoid compounds in the active fraction. The radical scavenging and in vitro diabetic related enzyme inhibitory activities were found to be dose dependent. The maximum ABTS⁺ and DPPH scavenging activity was documented in ethyl acetate fraction of the H. tuberosus followed by methanol extract, hexane fraction, and methanol fraction. We also found that H. tuberosus showed a less toxicity in mouse fibroblast cells and enhance the glucose uptake in insulin-resistant HepG2 cells. Besides, the ethyl acetate fraction of the H. tuberosus analyzed by UPLC-QTOF-MS-MS and GC/MS revealed the presence of phenolic compounds such as neochlorogenic acid, chlorogenic acid, caffeic acid, 5-O-(4-coumaroyl)-quinic acid, feruloylquinic acid, caffeoylquinic acid, isoxazolidine, salicylic acid β-D-glucoside, dicaffeoylquinic acid isomers, salvianolic acid derivative isomers, and 1,4 dicaffeoylquinic acid etc. Among the identified phytochemicals, six were chosen for molecular docking study to explore their its inhibitory interactions with α-amylase and α-glucosidase. Taken together, the findings of the present study suggested that phytocompounds of EAF were responsible for the significant in vitro antioxidant, wound-healing, and anti-diabetic activities.

In this work, a total of six polysaccharides were isolated from culture filtrate (EPS1, EPS2) and mycelia (IPS1–IPS4) of Trichoderma harzianum. The HPLC analysis results showed that EPS1, EPS2, IPS1, and IPS2 were composed of mannose, ribose, glucose, galactose, and arabinose. The FT-IR, ¹H, and ¹³C NMR chemical shifts confirmed that the signals in EPS1 mainly consist of (1→4)-linked α-d-glucopyranose. EPS1 and IPS1 showed a smooth and clean surface, while EPS2, IPS2, and IPS3 exhibited a microporous structure. Among polysaccharides, EPS1 displayed higher ABTS⁺ (47.09 ± 2.25% and DPPH (26.44 ± 0.12%) scavenging activities, as well as higher α-amylase (69.30 ± 1.28%) and α-glucosidase (68.22 ± 0.64%) inhibition activity than the other polysaccharides. EPS1 exhibited high cytotoxicity to MDA-MB293 cells, with an IC₅₀ of 0.437 mg/mL, and this was also confirmed by cell staining and FACS assays. These results report the physicochemical and bioactive properties of polysaccharides from T. harzianum.

Non-small cell lung cancer (NSCLC) is one of the leading causes of cancer-related mortality; thus, therapeutic targets continue to be developed. Anoctamin1 (ANO1), a novel drug target considered for the treatment of NSCLC, is a Ca²⁺-activated chloride channel (CaCC) overexpressed in various carcinomas. It plays an important role in the development of cancer; however, the role of ANO1 in NSCLC is unclear. In this study, diethylstilbestrol (DES) was identified as a selective ANO1 inhibitor using high-throughput screening. We found that DES inhibited yellow fluorescent protein (YFP) fluorescence reduction caused by ANO1 activation but did not inhibit cystic fibrosis transmembrane conductance regulator channel activity or P2Y activation-related cytosolic Ca²⁺ levels. Additionally, electrophysiological analyses showed that DES significantly reduced ANO1 channel activity, but it more potently reduced ANO1 protein levels. DES also inhibited the viability and migration of PC9 cells via the reduction in ANO1, phospho-ERK1/2, and phospho-EGFR levels. Moreover, DES induced apoptosis by increasing caspase-3 activity and PARP-1 cleavage in PC9 cells, but it did not affect the viability of hepatocytes. These results suggest that ANO1 is a crucial target in the treatment of NSCLC, and DES may be developed as a potential anti-NSCLC therapeutic agent.