Comparative Neuroprotective Effects of Moringa oleifera Seed Oil and Aqueous Extract on Cognitive Functions on a High-Fat, High-Fructose Diet Mice: Focus on Senescence Markers.

Several studies have demonstrated that Moringa oleifera (MO) has different pharmacological properties, including neuroprotective effects. However, the role of MO in preventing brain impairment in high-fat, high-fructose diet (HFFD) remains unknown. This study aimed to investigate the neuroprotective effects of MO leaves aqueous extract (MOE) and moringa seed oil (MOO) against brain impairment in mice with HFFD. Twenty-eight male mice were randomly divided into four groups: normal diet, HFFD, HFFD + MOE 500 mg/kgBW, and HFFD + MOO 2 mL/kgBW. Cognitive function was assessed using the Y-maze and novel object recognition (NOR) tests. The p16, p21, and BDNF expressions were analyzed using the RT-PCR method. Senescence-associated beta-galactosidase (SA-ß-gal) staining in the brain was also performed. The results showed that administration of MOE or MOO could increase the percentage of alternation and recognition of new objects, prevent the increase of p16 and p21 expression, and ameliorate SA-ß-Gal activity in the brain. MOO, but not MOE, increased BDNF expression in senescence brains isolated from HFFD mice. The findings indicate that MOO and MOE possess neuroprotective properties, with MOO demonstrating a greater ability to inhibit the brain senescence process compared to MOE.

Effect of Roselle Flower Extract (Hibiscus sabdariffa Linn.) on Reducing Steatosis and Steatohepatitis in Vitamin B12 Deficiency Rat Model.

Background and Objectives: Non-alcoholic Fatty Liver Disease (NAFLD) can occur as a result of micronutrient deficiencies. Hibiscus sabdarifa, a plant used in traditional medicine, contains ingredients that can help prevent this process. This study looked at the potency of Hibiscus sabdariffa Ethanol Extract (HSE) to prevent homocysteine-induced liver damage in animals that were deficient in vitamin B12. Materials and Methods: A comparative study of the effects of roselle extract is presented in an experimental design. Thirty Sprague-Dawley rats were divided into six groups using randomization. To demonstrate the absence of liver damage in the experimental animals under normal conditions, a control group was fed a normal diet without HSE. For the induction of liver damage in the experimental animals, the vitamin B12-restricted group was administered a vitamin B12-restricted diet. To test the effect of HSE on liver damage, the treatment group was given HSE along with a vitamin B12-restricted diet. Each group was given two treatment periods of eight and sixteen weeks. These results were compared with the results of the parameter examination between the vitamin B12 restriction group, with and without HSE, using an ANOVA statistic. The data were analyzed with licensed SPSS 20.0 software. Results: HSE significantly increased the blood levels of vitamin B12 while lowering homocysteine levels. The administration of HSE reduced liver damage based on the activity of liver function enzymes in the plasma due to a limitation of vitamin B12. HSE decreased Sterol Regulatory Element-Binding Protein-1c (SREBP1c) and Nuclear Factor Kappa B (NFkB) protein expressions in the liver tissue, but did not decrease Glucose-Regulated Protein 78 (GRP78) protein expression. Significantly, the levels of Tumor Necrosis Factor alpha (TNF-a) and IL-6 in the liver tissue were lower, while the levels of IL-10 and Nuclear factor-erythroid-2 Related Factor 2 (NRF2) were higher with HSE administration. HSE produced a better histopathological profile of the Hematoxylin and Eosin (H&E)-Masson tricrome for inflammation, fat and fibrosis in the liver. Conclusions: In this study, HSE was found to slow the development of liver damage in experimental animals that were given a vitamin B12-deficient diet.

Selected Indonesian Medicinal Plants for the Management of Metabolic Syndrome: Molecular Basis and Recent Studies.

Increased prevalence of metabolic syndrome (MetS) in the world influences quality of health in all respective countries, including Indonesia. Data from Indonesian Family Life Survey reported in 2019 showed that the prevalence of MetS in Indonesia currently is 21.66%, estimated with the provincial incidence ranging up to 50%; additionally, the most common components of MetS discovered in Indonesia were poor high-density lipoprotein (HDL) cholesterol and hypertension. Management treatment of MetS involves a combination of lifestyle changes and pharmacological interventions to decrease cerebrovascular disease. Various natural substances have been shown to govern any cardiovascular or metabolic disorders through different mechanisms, such as triggering anti-inflammation, lipid profile correction, sensitization of insulin reception, or blood glucose control. In Indonesia, the utilization of natural compounds is part of the nation's culture. The community widely uses them; even though in general, their effectiveness and safety have not been thoroughly assessed by rigorous clinical trials. Scientific evidence suggested that cinnamon, mangosteen, and curcumin, as well as their derived components possess a broad spectrum of pharmacological activity. In this review, an enormous potential of cinnamon, mangosteen, and curcumin, which originated and are commonly used in Indonesia, could be treated against MetS, such as diabetes, hyperlipidemia, hypertension, and obesity. The findings suggested that cinnamon, mangosteen, curcumin and their derivatives may reflect areas of promise in the management of MetS.

Anti-Diabetic Potential of Murraya Koenigii (L.) and its Antioxidant Capacity in Nicotinamide-Streptozotocin Induced Diabetic Rats.

AIM AND OBJECTIVE: The present study aims to investigate whether the antihyperglycemic effect of Murraya koenigii is mediated by antioxidant properties and insulin mimetic effect. METHODS: Thirty Spraque-Dawley rats were induced hyperglycemia by streptozotocin and nicotinamide (STZ-NA). The STZ-NA diabetic rats were treated with an ethanolic extract of Murraya koenigii 200 mg/kg b.w and 400 mg/kg b.w. One group was treated with glibenclamide (1 mg/kg b.w). After the administration of Murraya koenigii extract and glibenclamide for four weeks, the rats were sacrificed. Blood and organ samples were collected under a fasting condition. The body weight and blood glucose levels were measured. Hepatic enzymes were determined using a commercial kit, protein levels were estimated by Bradford's method, and plasma insulin was assayed by an ELISA kit. Malondialdehyde (MDA) and reduced glutathione (GSH) levels were estimated by the TBA-Wills method and Ellman's method, respectively. RESULTS: Ethanolic extract of Murraya koenigii showed a significant reduction in blood glucose level at both doses, 200 and 400 mg/kg b.w. In addition, Murraya koenigii exhibited a profound antioxidant effect with decreased MDA level and increased GSH level, particularly at the 200 mg/kg b.w. and significantly decreased the HOMA-IR index. CONCLUSIONS: The present study reveals that Murraya koenigii possesses antidiabetic activity and antioxidant effects on STZ-NA induced diabetes mellitus.

Curcumin attenuates diabetic nephropathy by inhibiting PKC-α and PKC-ß1 activity in streptozotocin-induced type I diabetic rats.

SCOPE: We hypothesized that curcumin, a potent anti-oxidant, might be beneficial in ameliorating the development of diabetic nephropathy through inhibition of PKC-α and PKC-ß1 activity-ERK1/2 pathway. METHODS AND RESULTS: Diabetes was induced by a single intraperitoneal injection of streptozotocin (STZ) (55 mg/kg) in rats. Three weeks after STZ injection, rats were divided into three groups, namely, normal, diabetic and diabetic treated with curcumin at 100 mg/kg/day, p.o., for 8 wk. At 11 wk after STZ injection, diabetic rats exhibited renal dysfunction, as evidenced by reduced creatinine clearance, increased blood urea nitrogen (BUN) and proteinuria, marked increases in lipid peroxidation, NOX4 and p67phox and decrease in anti-oxidant enzyme. All of these abnormalities were significantly reversed by curcumin. Furthermore, the high-glucose-induced PKC-α and PKC-ß1 activities and phosphorylated ERK1/2 was significantly diminished by curcumin. Curcumin also attenuated the expression of TGF-ß1, CTGF, osteopontin, p300 and ECM proteins such as fibronectin and type IV collagen. The high-glucose-induced expression of VEGF and its receptor VEGF receptor II (flk-1) was also ameliorated by curcumin. CONCLUSION: These results prove that curcumin produces dual blockade of both PKC-α and PKC-ß1 activities, which suggests that curcumin is a potential adjuvant therapy for the prevention and treatment of diabetic nephropathy.

The antioxidant edaravone attenuates ER-stress-mediated cardiac apoptosis and dysfunction in rats with autoimmune myocarditis.

Experimental autoimmune myocarditis (EAM) is mediated by myocardial infiltration by myosin-specific T-cells secreting inflammatory cytokines. In this study, rat models of EAM were prepared by injection with porcine cardiac myosin. One week after immunization, edaravone was administered intraperitoneally at 3 or 10 mg/kg/day to rats for 2 weeks. Cardiac function was measured by haemodynamic and echocardiographic studies and TUNEL assay was performed. Left ventricular (LV) expression of NADPH oxidase sub-units (p47(phox) and p67(phox)), pro-inflammatory cytokines (TNF-alpha), endoplasmic reticulum (ER) stress signalling proteins (GRP78, caspase-12 and GADD153) and mitogen-activated protein kinase (MAPK) family proteins (phospho-p38 MAPK and phospho-JNK) were measured by western blotting. Edaravone improved LV function in a dose-dependent manner. Central venous pressure was significantly low and LV ejection fraction and fractional shortening was significantly high in edaravone groups compared with those in the vehicle group. In addition, edaravone treatment down-regulated LV expressions of p47(phox), TNF-alpha, GADD153, phospho-p38 MAPK and phospho-JNK. Furthermore, the LV expressions of p67(phox), GRP78, caspase-12 and TUNEL-positive cells of rats with EAM treated with edaravone were significantly low compared with those of the vehicle group. These findings suggest that edaravone ameliorated the progression of EAM by inhibiting oxidative and ER stress and, subsequently, cardiac apoptosis.