Background Hypercholesterolemia is a major risk factor for cardiovascular disease. It has been reported that pineapple contains healthy nutrients and phytochemicals associated with antioxidant and anti-inflammatory capacities. No investigation exists concerning the effect of pineapple consumption modulating hypercholesterolemia-induced cardiac damage in high-cholesterol diet (HCD)-fed rats. This study evaluated the effect of pineapple consumption on lipid-lowering, cardiac oxidative stress and inflammation in HCD-fed rats. Methods Male Sprague–Dawley rats were fed with HCD, in the presence and absence of Pineapple (Ananas comosus L.) cv. Pattavia powder for 8 weeks. Then, serum lipid profiles, liver and renal function tests, cardiac oxidative stress and pro-inflammatory cytokines were determined. Results Daily pineapple consumption reduced weight gain, serum lipid profiles, atherogenic coefficient (AC), cardiac risk ratio (CRR), and liver enzyme activity, without causing renal dysfunction. Pineapple consumption also restores cardiac protein carbonyl (cPC) content, reduces cardiac malondialdehyde (MDA), cardiac pro-inflammation cytokine IL-6 and IL-1β levels. Conclusion Pineapple possesses antioxidant and lipid-lowering properties and daily consumption alleviates hypercholesterolemia-induced cardiac lipid peroxidation and pro-inflammation elevation in an in vivo model. This study demonstrates that pineapple is a potential candidate for cardioprotection against hypercholesterolemia.

BackgroundHypercholesterolemia is an independent modifiable risk factor that accelerates the development of both non-alcoholic fatty liver and atherosclerosis. Coconut water contains a variety of phytochemicals that make it appealing for producing vinegar. Coconut vinegar is rapidly gaining popularity for health benefits in Southeast Asia. The purpose of this study is to evaluate the effect of daily supplementation of coconut vinegar on hepatic and vascular oxidative stress in rats fed a high-cholesterol diet (HCD).MethodsMature coconut water was fermented with coconut sap sugar using Saccharomyces cerevisiae and Acetobacter aceti vat Europeans, respectively. Bioactive compounds and antioxidant capacity of coconut vinegar were examined in vitro. Adult male Sprague–Dawley rats were randomly divided into four groups; the control group fed a standard diet (S), a group that received HCD (SC), a group that received HCD supplemented with coconut vinegar at a dose of 1 mL/kg/day (SCV), and a group that received HCD with atorvastatin at a dose of 30 mg/kg/day (SCA). After 8 weeks, serum metabolic profiles, fatty liver, hepatic, and vascular oxidative stress were determined.ResultsIn in vitro studies, coconut vinegar was rich in phenolic compounds and organic acids. The antioxidant capacity of 30 μL of coconut vinegar was 181.55 ± 8.15 μM Trolox equivalent antioxidant capacity (TEAC). In the HCD fed rats, daily supplementation of coconut vinegar reduced weight gain, serum triglycerides, and fasting blood sugar levels without renal or liver toxicity. In the liver, coconut vinegar reduced the accumulation of both hepatic cholesterol and hepatic triglyceride, and it also reduced hepatic 4-hydroxynonenal (4-HNE) lipid peroxidation. In the aortic tissues, coconut vinegar increased nitric oxide bioavailability and reduced aortic 4-HNE lipid peroxidation.ConclusionNovel coconut vinegar is the source of antioxidants, and daily supplementation of coconut vinegar was found to attenuate dyslipidemia-induced hepatic and vascular oxidative stress by protective against cellular lipid peroxidation.

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Damage-associated molecular patterns (DAMPs) are well recognized as the molecular signature of immunogenic cell death (ICD). The efficacy of drug-induced ICD function may be impacted by the precise ratio between immunostimulatory and immunoinhibitory DAMPs. Tumor-derived DAMPs can activate tumor-expressed TLRs for the promotion of tumor cell motility, invasion, metastatic spread and resistance to chemotherapeutic treatment. Herein, drug-induced DAMPs’ expression and their role in tumor progression are utilized as one crucial point of evaluation regarding chemotherapeutic treatment efficacy in our study. Cisplatin and oxaliplatin, the conventional anticancer chemotherapy drugs, are emphasized as a cause of well-known DAMPs’ release from cholangiocarcinoma (CCA) cells (e.g., HSP family, S100, CRT and HMGB1), whereby they trigger Akt, ERK and Cyclin-D1 to promote tumor activities. These findings strengthen the evidence that DAMPs are not only involved in immunomodulation but also in tumor promotion. Therefore, DAMP molecules should be considered as either targets of cancer treatment or biomarkers to evaluate treatment efficacy and tumor recurrence.

Hypercholesterolaemia is a significant risk factor for developing vascular disease and fatty liver. Pineapple (Ananas comosus), a tropical fruit widely cultivated in Asia, is reported to exhibit antioxidant and cholesterol-lowering...