Dengue is a vector-borne disease caused by the dengue virus (DENV) of family Flaviviridae. Dengue fever is common in both developed and developing countries. Globally, approximately 400 million cases of dengue fever are reported annually, resulting in approximately 22 000 fatalities. Dengue cases in India have progressively increased in the last decade. In recent years, substantial progress has been made in understanding various aspects of dengue, including its pathogenesis, diagnosis, prevention strategies, immunological responses, and the role of vectors in its transmission. The transmission of a positive RNA virus occurs through Aedes mosquitoes, specifically Aedes aegypti and Aedes albopictus. This virus is associated with a wide spectrum of symptoms, ranging from mild undifferentiated fever to severe hemorrhagic fever and shock, posing a potential threat to human health. There are 4 types of antigenically distinct dengue serotypes (DENV-1 to DENV-4) and among them, DENV-2 is more lethal and extremely severe. To overcome the severity of dengue, Dengvaxia is administered to children 9 to 16 years old with evidence of previous dengue infection. The diagnosis of dengue is carried out by ELISA-based non-structural protein (NS1) and immunoglobulin tests. However, there are no specific biomarkers to identify severe disease progression. Climatic factors and temperature play an important role in complex interaction among host, vector, and virus to manifest the severity of dengue. There is a need for the refinement of climate-based disease forecasting models in India to effectively control the spread of dengue. The mosquito repellent should be used periodically to kill or repel the Aedes mosquito to prevent the spread of dengue in humans.

Objective: To evaluate the effects of an aqueous extract of Protaetia brevitarsis (AEPB) on the growth of zebrafish and preosteoblast MC3T3-E1 cells. Methods: The effects of AEPB on the linear growth and the expression of growth-related genes in zebrafish and MC3T3-E1 cells were assessed using various molecular techniques. Furthermore, the involvement of the mammalian target of rapamycin (mTOR) pathway in AEPB-induced growth was investigated by employing the mTOR inhibitor rapamycin. Results: AEPB administration led to a significant and dose-dependent increase in zebrafish larvae growth over time. Additionally, AEPB treatment upregulated the expression of growth hormone-1 (GH-1), insulin-like growth factor-1 (IGF-1), growth hormone receptor-1 (GHR-1), and cholecystokinin-a (CCKA) in zebrafish. Similarly, AEPB stimulated the expression and release of IGF-1 and accelerated mTOR expression in MC3T3-E1 cells. In addition, rapamycin hindered AEPB-induced linear growth in zebrafish larvae and suppressed the expression of growth-promoting genes by inhibiting mTOR activation. Conclusions: AEPB shows growth-promoting effects by upregulating growth-related genes and activating the mTOR signaling pathway. Further investigations are warranted to elucidate its mechanisms of action and explore its potential application in the development of growth-enhancing supplements for various purposes.

Objective: To evaluate the effect of hydroxysafflor yellow A (HSYA) on thioacetamide-induced liver fibrosis. Methods: Thioacetamide was administered to rats intraperitoneally in doses of 200 mg/kg twice a week for 12 weeks. Thioacetamide-intoxicated rats were given silymarin (50 mg/kg) or HSYA (5 mg/kg) orally every day for 8 weeks. Liver enzymes, fibrosis markers, histological changes as well as immunohistochemistry of TNF-α, IL-6, p21, α-SMA, and caspase-3 were examined. The effect of HSYA on HSC-T6 activation/proliferation and apoptosis was also determined in vitro. Results: HSYA decreased liver enzymes, TNF-α, IL-6, and p21 expressions, hepatic PDGF-B, TIMP-1, TGF-β1, and hydroxyproline levels, as well as fibrosis score (S2 vs. S4) compared to the thioacetamide group. HSYA also downregulated α-SMA while increasing caspase-3 expression. Surprisingly, at 500 µg/mL, HSYA had only a slightly suppressive effect on HSC proliferation, with a 9.5% reduction. However, it significantly reduced TGF-β1, inhibited α-SMA expression, induced caspase-3 expression, and promoted cell senescence. Conclusions: HSYA may be a potential therapeutic agent for delaying and reversing the progression of liver fibrosis. More research on HSYA at higher doses and for a longer period is warranted.

Objective: To comparatively investigate the ameliorative effect of Phellinus igniarius (P. igniarius) on renal aging in a rat model of focal and segmental glomerulosclerosis (FSGS). Methods: The FSGS model was established in rats by uninephrectomy combined with tail vein injection of doxorubicin. The FSGS rats were randomly divided into the model group, the P. igniarius decoction group, the P. igniarius polysaccharides group, and the P. igniarius polyphenols group. Molecular indicators of cell senescence, renal function indexes, and podocyte injury markers were tested after ten weeks of intragastric administration. Besides, the pathological renal lesions and the ultrastructural changes were observed. Results: FSGS developed in the model group within ten weeks and showed segmental glomerular scarring and renal aging. Following the 10-week intervention, 24 h proteinuria, serum creatinine, blood urea nitrogen, P16^INK4α, thrombospondin-1, and transforming growth factor-β1 were decreased in each treatment group, whereas albumin, erythropoietin, nephrin, and podocin were increased; the pathological renal injury was alleviated, and the number of senescent cells was reduced, especially in rats treated with P. igniarius decoction. Conclusions: P. igniarius ameliorates renal aging and renal injury in the FSGS rat model. Compared with the effective constituents (polysaccharides and polyphenols), P. igniarius decoction has a better curative effect, which is expected to provide a new therapeutic idea for FSGS.