Asian Pacific Journal of Tropical Biomedicine

325-338

Authors: Sahu, Mahesh Chandra; Samantaray, Rakesh Kumar; Pal, Aditi; Pati, Sanghamitr

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 22000 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.

348-358

Authors: Seif el-Din, Sayed H.; Hammam, Olfat A.; Ezzat, Shahira M.; Saleh, Samira; Safar, Marwa M.; El-Maadawy, Walaa H.; El-Lakkany, Naglaa M.

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.