Pandanus tectorius fruits have been used as major food in Micronesia, but not fully exploited in South East Asia. In Malaysia and Indonesia, P. tectorius fruit is wasted and still not utilized either as a source of food as well as for research. The aims of the present study were to determine the phytochemical content, antibacterial and antioxidant activities, total phenolic content (TPC) and cytotoxicity properties of cores and keys parts of P. tectorius fruits extracts against some normal (RAW and L-6) and cancer cell lines (HeLa, HepG2 and MCF-7). Samples were collected from Setiu Wetland, Terengganu, Malaysia. Extracts were obtained by successive extraction using hexane, ethyl acetate and methanol. The antibacterial activity was performed by disk diffusion method against gram positive (Bacillus subtilis and Staphylococcus aureus) and gram negative (Escherichia coli, and Pseudomonas aeruginosa) bacteria. Actives extract was continued for antibacterial kinetic study. The TPC and antioxidant were analyzed by Folin–Ciocalteu and DPPH free radical scavenging assay, respectively. Qualitative phytochemical analysis result confirmed the presence of phenolics, flavonoids, terpenoid, steroids, saponins and glycosides as chemical constituents in P. tectorius fruits extract. It was supported by high TPC content in this extracts. The ethyl acetate extract from cores part (PEC) showed the highest antioxidant capacity (IC50=0.8±0.20mg/mL), while ethyl acetate extract from keys part (PEK) displayed highest antibacterial activity with inhibition zone of 10–15mm, but less strong inhibition as compared to the investigated commercial antibiotics (ampicillin, penicillin, gentamycin, and tetracycline). Antibacterial kinetic study was further proven that PEK has good antibacterial activity. Moreover, cytotoxicity study revealed that all of extracts did not have any cytotoxic activity against all selected cell lines (IC50 value>30μg/mL). Result founded that both keys and core parts of P. tectorius fruits were found to be rich by phenolics content and potent as antioxidant and antibacterial agents. Since it is not toxic against selected cell lines, the mechanism study on antiinflammatory, antidiabetic, antiatherosclerosis could be carried out

The present study comprised of the synthesis of dicyanoaniline derivatives of pyridine, thiophene, furan, and substituted phenyl 1-29. All synthetic derivatives were evaluated for their potential to inhibit α-amylase and α-glucosidase enzymes. The synthesized compounds are classified into three categories A, B, and C based on variable substituents at R₁ and R_2, and the structure-activity relationship was discussed accordingly. Amongst twenty-nine derivatives, 1-29, five compounds 2, 9, 18, 23, and 24 displayed excellent inhibition against α-amylase and α-glucosidase enzymes with the IC₅₀ values ranging between 20.33 ± 0.02-25.50 ± 0.06 µM and 21.01 ± 0.12-27.75 ± 0.17 µM, respectively, while other compounds showed moderate to weak inhibition against both enzymes. Acarbose was used as the positive control in this study. The enzyme kinetic studies showed non-competitive and un-competitive types of inhibition mechanism against α-amylase and α-glucosidase enzymes, respectively. In silico studies have demonstrated the involvement of these molecules in numerous binding interactions within the active site of the enzyme.

One of the pathways to reduce cholesterol production in the liver is through the inhibition of HMG-Coa reductase (HMGCR) by current drugs, statins. However, these have side effects if consumed in prolonged periods. Tangeretin and trans-ethyl caffeate as alternative drugs in reducing hypercholesterolemia and preventing atherosclerosis have never been reported. Their effects on inhibiting HMGCR activity were investigated through enzymatic method (in vitro and in vivo). The toxicity property was analyzed on the Serum Glutamate Oxalate Transaminase (SGOT)/Serum Glutamate Piruvate Transaminase (SGPT) levels and rat liver histology. The results showed that both compounds inhibited HMGCR activity significantly compare to the control simvastatin (p < 0.05). Tangeretin which showed very good activity in inhibiting HMGCR (83.8 of % inhibition, equal to simvastatin) was selected and used for anti-hypercholesterolemia in vivo assessment. Furthermore, tangeretin was shown to effectively reduced Total Cholesterol (TC) and Low Density Lipoprotein (LDL), and increased High Density Lipoprotein (HDL) levels significantly compared to the simvastatin group (p < 0.05). Tangeretin group was also proven to inhibit HMGCR rat liver activity significantly compare to the control simvastatin (p < 0.05). The toxicity study on the SGOT/SGPT levels and liver histology revealed that there were no side effects after administration by tangeretin. Results found that both tangeretin and trans-ethyl caffeate are potent candidates as anti-hypercholesterolemia agent in vitro. In addition, tangeretin was also shown to be safe and suitable as an alternative treatment for controlling hypercholesterolemia in vivo as well as have potency for preventing atherosclerosis.

In vitro and in vivo studies of the activity of Phaleria macrocarpa Boerl (Thymelaeaceae) leaves against the therapeutic target for hypercholesterolemia were done using the HDL receptor (SR-BI) and hypercholesterolemia-induced Sprague Dawley rats. The in vitro study showed that the active fraction (CF6) obtained from the ethyl acetate extract (EMD) and its component 2',6',4-trihydroxy-4'-methoxybenzophenone increased the SR-BI expression by 95% and 60%, respectively. The in vivo study has proven the effect of EMD at 0.5 g/kgbw dosage in reducing the total cholesterol level by 224.9% and increasing the HDL cholesterol level by 157% compared to the cholesterol group. In the toxicity study, serum glutamate oxalate transaminase (SGOT) and serum glutamate pyruvate transaminase (SGPT) activity were observed to be at normal levels. The liver histology also proved no toxicity and abnormalities in any of the treatment groups, so it can be categorized as non-toxic to the rat liver. The findings taken together show that P. macrocarpa leaves are safe and suitable as an alternative control and prevention treatment for hypercholesterolemia in Sprague Dawley rats.

Pandanus tectorius fruit, a natural product rich in tangeretin and ethyl caffeate, has been reported to have potential as anti-hypercholesterolemia agent via Scavenger Receptor Class B type 1 (SR-B1) pathway. However, due to its semi-polar properties, P. tectorius extract exhibits poor solubility when used as a medical remedy. The extract’s solubility can potentially be improved through a synthesis of nanoparticles of chitosan-P. tectorius fruit extract. This can also increase the extract’s SR-B1 gene expression activity. To date, no studies of nanoparticles of chitosan-P. tectorius fruit extract and its pathway via SR-B1 have been published anywhere. In this study, cytotoxicity properties against HepG2 were explored by MTT. Then luciferase assay was used to detect their effectiveness in increasing SR-B1 activity. An in vivo study using Sprague dawley was carried out to observe the extract nanoparticles’ effectiveness in reducing the cholesterol levels and the toxicity property in rat’s liver. As the results showed, the extract nanoparticles had no cytotoxic activity against HepG2 cells and exhibited higher SR-B1 gene expression activity than the non-nanoparticle form. As the in vivo study proved, nanoparticle treatment can reduce the levels of TC (197%), LDL (360%), and TG (109%), as well as increase the level of HDL cholesterol by 150%, in comparison to those for the untreated high-cholesterol diet group. From the toxicity study, it was found that there was non-toxicity in the liver. It can be concluded that nanoparticles of chitosan-P. tectorius fruit extract successfully increased P. tectorius fruit extract’s effectiveness in reducing hypercholesterolemia via SR-B1 pathway. Hence, it can be suggested that nanoparticles of chitosan-P. tectorius fruit extract is safe and suitable as an alternative treatment for controlling hypercholesterolemia via SR-B1 pathway.