Objective: To assess aptamer-based assays for diagnosing latent tuberculosis infection (LTBI).

Methods: Literature from Medline, ScienceDirect, and Scopus, covering publications from January 1, 2012, to December 31, 2023, was examined. This review evaluates different aptamers, biomarkers, sample types, sample sizes, reference assays, and the assays’ sensitivity and specificity. By using the Quality Assessment of Diagnostic Accuracy Studies 2, the risk of bias in each study was evaluated.

Results: Aptamer-based assays generally showed a sensitivity of 90% (95% CI: 75%-100%) and specificity of 90% (95% CI: 50%-100%), where optical aptasensor showed the highest sensitivity and specificity at 100%. Serum samples were frequently used to enhance antigen detectability, improving the assay’s performance. Meanwhile, HspX was the most studied biomarker, followed by MPT64, and IFN-γ.

Conclusions: Aptamer-based assays could be reliable alternatives to current LTBI detection methods, but further research is needed to validate their clinical efficacy.

Objective: To investigate the osteogenic effects of polyphenol-rich extracts from Wisteria floribunda (Willd.) DC. (W. floribunda) flowers and elucidate the underlying mechanisms.

Methods: Polyphenolic compounds of W. floribunda extracts were analyzed, including flavonoids and glucoside derivatives. Osteogenic activity was assessed in MC3T3-E1 preosteoblast cells by measurement of alkaline phosphatase (ALP) activity, alizarin red S staining, and the expression of osteogenic markers (RUNX2, SP7, and ALPL). In vivo effects were evaluated in zebrafish larvae by assessing skeletal development and expression of osteogenic genes (runx2a, sp7, and alpl). The role of mammalian target of rapamycin (mTOR) pathway was examined using rapamycin.

Results: W. floribunda extracts significantly enhanced ALP activity, bone mineralization, and the expression of RUNX2, SP7, and ALPL in MC3T3-E1 cells. In zebrafish larvae, W. floribunda extracts improved vertebral mineralization and upregulated osteogenic genes. Mechanistically, the plant extract activated the mTOR pathway, and rapamycin treatment attenuated the extracts-induced ALP activity, mineralization, and vertebral formation in zebrafish, confirming mTOR involvement.

Conclusions: W. floribunda extracts promote osteoblast differentiation and bone formation via mTOR pathway activation. These findings provide novel insights into the potential of W. floribunda extracts and support its further investigation as a natural therapeutic candidate for bone degenerative disorders such as osteoporosis.

Objective: To investigate the protective effect of ursolic acid (UA) on isoproterenol (ISO)-induced kidney injury in mice.

Methods: Four groups of mice were used: Group I (Control) received phosphate-buffered saline i.p. for four weeks; Group II (ISO alone) was administered ISO (10 mg/kg i.p.) daily for four weeks to induce kidney injury; Group III (ISO+UA) was pretreated with UA (40 mg/kg i.p.) once daily, followed by ISO (10 mg/kg i.p.) once daily for four weeks; Group IV (UA alone) received UA (40 mg/kg i.p.) daily for four weeks. Markers of oxidative stress, inflammation, and apoptosis were analyzed, and the protein expression of p-PI3K and p-Akt was determined.

Results: UA treatment significantly alleviated ISO-induced kidney injury, evidenced by lowered levels of malondialdehyde, IL-6, TNF-α and IL-Iβ, downregulated expression of cleaved caspase-3 and PARP, and upregulated expression of Bcl-2 and Bcl-xL. It also activated the PI3K/Akt pathway.

Conclusions: UA demonstrates renoprotective effects against ISO-induced kidney injury by reducing oxidative stress, inflammation, and apoptosis, likely through PI3K/Akt pathway activation. These findings suggest that UA may serve as a potential therapeutic agent for renal diseases linked to inflammation and oxidative stress, meriting further exploration for clinical applications.

Objective: To explore the effect of alantolactone on thioacetamide-induced liver fibrosis in mice as well as elucidate its underlying mechanism.

Methods: Animals were divided into 5 groups: the control, the thioacetamide group (150 mg/kg/twice weekly), the thioacetamide groups treated with alantolactone (5 and 10 mg/kg) or silymarin (50 mg/kg), respectively. All treatments were continued for 6 successive weeks, followed by collection of sera and tissue samples. Biochemical, histological, and immunohistochemical analyses were performed to examine the hepatoprotective effects of alantolactone.

Results: Alantolactone ameliorated thioacetamide-induced hepatic impairment and prevented the rise of serum activities of liver enzymes. Its hepatoprotective effect was further confirmed by histological examinations. Moreover, alantolactone lowered the expression of transforming growth factor-beta 1 and alpha-smooth muscle actin, hydroxyproline content as well as COL1A1 mRNA expression. It restored antioxidant balance and inhibited thioacetamide-induced upregulated expression of interleukin-1 beta, interleukin-6, and tumor necrosis factor-alpha, Toll-like receptor 4 (TLR4), myeloid differentiation primary response 88 (MyD88), and nuclear factor kappa B (NF-κB).

Conclusions: Alantolactone protects against thioacetamide-induced liver fibrosis in mice by reducing collagen deposition, oxidative stress, and inflammation. These effects are mediated, at least partly, by the inhibition of TLR4/MyD88/NF-κB axis.

Objective: To examine the effect of shikonin against streptozotocin (STZ)-induced diabetic retinopathy in rats and elucidate the underlying mechanisms.

Methods: Intraperitoneal administration of STZ (65 mg/kg) was used for the induction of diabetic retinopathy in rats. Rats received oral administration of shikonin (10, 20, and 30 mg/kg). The blood glucose level, insulin, body weight, and organ weight were estimated. Advanced glycation end products (AGEs) levels in serum and lens as well as protein carbonyl content of the lens were determined. The parameters related to oxidative stress and inflammation, and the levels of nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule 1 (VCAM-1) were also measured. In addition, quantitative RT-PCR was performed to determine the mRNA expressions.

Results: Shikonin treatment decreased glucose level and boosted insulin level, along with an increase in body weight and improved organ weight. It also lowered O2•-, ONOO-, serum and lens AGEs, and protein carbonyl content. Furthermore, shikonin treatment significantly alleviated oxidative stress and inflammation, as evidenced by reduced malonaldehyde, nitric oxide, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6, cyclooxygenase-2, prostaglandin E2, protein carbonyl content, and nuclear factor kappa-B, and increased superoxide dismutase, glutathione, catalase, and glutathione peroxidase. Markedly decreased levels of ICAM-1 and VCAM-1, as well as heightened levels of Nrf2 and HO-1, were noticed after treatment with shikonin. Furthermore, the mRNA expressions of TNF-α, IL-1β, IL-6, ICAM-1, VCAM-1, RAGE, collagen IV, and fibronectin were significantly downregulated.

Conclusions: Shikonin exhibits protective effects against STZ-induced diabetic retinopathy in rats via modulating the Nrf2/HO-1 and NF-κB signaling pathways.