Hesperidin

1 Citrus sp. 2 Daphne sp. 3 Galium sp. 4 Hyssopus sp. 5 Mentha sp. 6 Rosmarinus sp. 7 Scrophularia sp. 8 Valeriana sp. 9 Verbascum sp. 10 Zanthoxylum sp.

Hesperidin (HP) is a bioflavonoid that plays a role in plant defense and is abundant in citrus species, such as grapefruit, lemon and orange. Hesperidin is used effectively as a supplemental agent in complementary therapy protocols, since it possesses biological and pharmacological properties as an effective antioxidant, anti-inflammatory, anti-carcinogenic, and anti-hypertensive agent with lipid-lowering activity[1] IC50: hesperidin (IC50=116.68μmo/L))[4] in vitro: hesperidin and linarin are two of the main constituent of Valeriana's extract exhibiting a high affinity to KATP channel, which are related to the control of Ca++ concentration and release of GABA in synaptic nerve terminal, mainly on cells of SN[2] in vivo: Hesperidin was dissolved in 1% carboxymethyl cellulose (CMC) and administered orally at a dose of 50 mg/kg for 10 consecutive days. In the control group, rats were treated with the corn oil and 1% CMC vehicle.[1]

References:
[1]. Asli Cetin, Ali Otlu et al. Protective effect of hesperidin on oxidative and histological liver damage following carbon tetrachloride administration in Wistar rats. Arch Med Sci, 2016 Jun 1, 12(3): 486-493. [2]. Gesivaldo Santos, Bruno Andrade et al. SUR1 Receptor Interaction with Hesperidin and Linarin Predicts Possible Mechanisms of Action of Valeriana officinalis in Parkinson. Front Aging Neurosci, 2016, 8: 97. [3]. Jin Zhang, Jing Gao et al. Hesperidin inhibits HeLa cell proliferation through apoptosis mediated by endoplasmic reticulum stress pathways and cell cycle arrest. BMC Cancer, 2015, 15: 682. [4]. Cetin A, Otlu A, ea al. Protective effect of hesperidin on oxidative and histological liver damage following carbon tetrachlorideadministration in Wistar rats. Arch Med Sci, 2016 Jun 1, 12(3):486-93.

Protective effect of hesperidin in a model of Parkinson's disease induced by 6-hydroxydopamine in aged mice.[Pubmed:25280422]

Nutrition. 2014 Nov-Dec;30(11-12):1415-22.

OBJECTIVE: Parkinson's disease (PD) may be caused by the interaction of a number of factors, including genetics, toxins, oxidative stress, mitochondrial abnormalities, and aging. Studies have shown that consumption of an antioxidant-rich diet may reduce the incidence of neurodegenerative diseases. The aim of this study was to evaluate the role of the flavonoid Hesperidin in an animal model of PD induced by 6-hidroxidopamine (6-OHDA). METHODS: Aged mice were treated with Hesperidin (50 mg/kg) during 28 d after an intracerebroventricular injection of 6-OHDA. The enzymatic activities of superoxide dismutase, catalase, glutathione reductase, glutathione peroxidase, and glutathione S-transferase, the levels of glutathione, reactive oxygen species, total reactive antioxidant potential, dopamine and its levels of metabolites 3,4-dihydroxyphenylacetic acid and homovanillic acid, was analyzed in the striatum. The behavioral parameters (depressive-like, memory, and locomotor) were measured. RESULTS: This study demonstrated that Hesperidin (50 mg/kg) treatment was effective in preventing memory impairment in the Morris water maze test, as well as, depressive-like behavior in the tail suspension test. Hesperidin attenuated the 6-OHDA-induced reduction in glutathione peroxidase and catalase activity, total reactive antioxidant potential and the dopamine and its metabolite levels in the striatum of aged mice. 6-OHDA increased reactive oxygen species levels and glutathione reductase activity in the striatum, and these alterations were mitigated by chronic administration of Hesperidin. CONCLUSION: This study demonstrated a protective effect of Hesperidin on the neurotoxicity induced by 6-OHDA in aged mice, indicating that it could be useful as a therapy for the treatment of PD.

Effect of hesperidin and neohesperidin from bittersweet orange (Citrus aurantium var. bigaradia) peel on indomethacin-induced peptic ulcers in rats.[Pubmed:24691249]

Environ Toxicol Pharmacol. 2014 May;37(3):907-15.

Hesperidin and neoHesperidin are the major flavanones isolated from bittersweet orange. It was recently reported that they have potent anti-inflammatory effects in various inflammatory models. In the present study, the effects of Hesperidin and neoHesperidin on indomethacin-induced ulcers in rats and the underlying mechanisms were investigated. Gastric ulcers were induced in rats with a single dose of indomethacin. The effects of pretreatment with Hesperidin and neoHesperidin were assessed in comparison with omeprazole as reference standard. Ulcer index, gene expression of gastric cyclooxygenase-2 (COX-2), tumor necrosis factor alpha (TNF-alpha), lipid peroxidation product, malondialdhyde (MDA), and reduced glutathione (GSH) content in stomach were measured. Furthermore, gross and histopathological examination was performed. Our results indicated that both Hesperidin and neoHesperidin significantly aggravated gastric damage caused by indomethacin administration as evidenced by increased ulcer index and histopathological changes of stomach.

Hesperidin induces apoptosis and triggers autophagic markers through inhibition of Aurora-A mediated phosphoinositide-3-kinase/Akt/mammalian target of rapamycin and glycogen synthase kinase-3 beta signalling cascades in experimental colon carcinogenesis.[Pubmed:25047426]

Eur J Cancer. 2014 Sep;50(14):2489-507.

Abnormalities in the homeostasis mechanisms involved in cell survival and apoptosis are contributing factors for colon carcinogenesis. Interventions of these mechanisms by pharmacologically safer agents gain predominance in colon cancer prevention. We previously reported the chemopreventive efficacy of Hesperidin against colon carcinogenesis. In the present study, we aimed at investigating the potential of Hesperidin over the abrogated Aurora-A coupled pro-survival phosphoinositide-3-kinase (PI3K)/Akt signalling cascades. Further, the role of Hesperidin over apoptosis and mammalian target of rapamycin (mTOR) mediated autophagic responses were studied. Azoxymethane (AOM) induced mouse model of colon carcinogenesis was involved in this study. Hesperidin treatment was provided either in initiation/post-initiation mode respectively. Hesperidin significantly altered AOM mediated anti-apoptotic scenario by modulating Bax/Bcl-2 ratio together with enhanced cytochrome-c release and caspase-3, 9 activations. In addition, Hesperidin enhanced p53-p21 axis with concomitant decrease in cell cycle regulator. Hesperidin treatment caused significant up-regulation of tumour suppressor phosphatase and tensin homologue (PTEN) with a reduction in the expression of AOM mediated p-PI3K and p-Akt. Additionally, Hesperidin administration exhibited inhibition against p-mTOR expression which in turn led to stimulation of autophagic markers Beclin-1 and LC3-II. Aurora-A an upstream regulator of PI3K/Akt pathway was significantly inhibited by Hesperidin. Furthermore, Hesperidin administration restored glycogen synthase kinase-3 beta (GSK-3beta) activity which in turn prevented the accumulation of oncoproteins beta-catenin, c-jun and c-myc. Taken together, Hesperidin supplementation initiated apoptosis via targeted inhibition of constitutively activated Aurora-A mediated PI3K/Akt/GSK-3beta and mTOR pathways coupled with autophagic stimulation against AOM induced colon carcinogenesis.

Hesperidin, a citrus flavonoid, inhibits bone loss and decreases serum and hepatic lipids in ovariectomized mice.[Pubmed:12771335]

J Nutr. 2003 Jun;133(6):1892-7.

The purpose of this study was to examine whether Hesperidin inhibits bone loss in ovariectomized mice (OVX), an animal model of postmenopausal osteoporosis. Forty 8-wk-old female ddY mice were assigned to five groups: a sham-operated group fed the control diet (AIN-93G), an OVX group fed the control diet, an OVX+HesA group fed the control diet containing 0.5 g/100 g Hesperidin, and an OVX+HesB group fed the control diet containing 0.7 g/100 g alpha-glucosylHesperidin and an OVX+17beta-estradiol (E(2)) group fed the control diet and administered 0.03 micro g E(2)/d with a mini-osmotic pump. After 4 wk, the mice were killed and blood, femoral, uterine and liver were sampled immediately. Hesperidin administration did not affect the uterine weight. In OVX mice, the bone mineral density of the femur was lower than in the sham group (P < 0.05) and this bone loss was significantly prevented by dietary Hesperidin or alpha-glucosylHesperidin. The Ca, P and Zn concentrations in the femur were significantly higher in the Hesperidin-fed and E(2) groups than in the OVX group. Histomorphometric analyses showed that the trabecular bone volume and trabecular thickness in the femoral distal metaphysis were markedly decreased (P < 0.05) by OVX, and alpha-glucosylHesperidin significantly prevented this bone loss. Furthermore, Hesperidin decreased the osteoclast number of the femoral metaphysis in OVX mice, as did E(2). Serum and hepatic lipids were lower in mice that consumed the Hesperidin-containing diets (P < 0.05) than in the OVX group fed the control diet. These results suggest a possible role for citrus flavonoids in the prevention of lifestyle-related diseases because of their beneficial effects on bone and lipids.

Protective effect of hesperidin against lung injury induced by intestinal ischemia/reperfusion in adult albino rats: histological, immunohistochemical and biochemical study.[Pubmed:25063207]

Tissue Cell. 2014 Oct;46(5):304-10.

Hesperidin is a naturally common flavonoid. It is an abundant and cheap by-product of citrus cultivation. It is reported to have antioxidative, anti-inflammatory and anticarcinogenic effects. This work was performed to investigate the possible protective role of Hesperidin in ameliorating the effect of experimentally induced intestinal ischemia/reperfusion injury (I/R) on lung tissue, histologically, immunohistochemically and biochemically. Thirty male Wistar adult albino rats were randomized into three groups named: group I (control group); group II (I/R); and group III (I/R with Hesperidin). Intestinal I/R was induced by occluding the superior mesenteric artery for 60 min, followed by 120 min of reperfusion period. Animals were given Hesperidin orally 1h before the onset of ischemia. At the end of the reperfusion period the lung tissues were extracted for histopathological examination and immunohistochemical detection of the distribution of inducible nitric oxide synthase (iNOS). Pulmonary edema was evaluated by lung tissue wet/dry weight ratios. The levels of malondialdehyde (MDA, a biomarker of oxidative damage), myeloperoxidase (MPO, an index of the degree of neutrophil accumulation) and glutathione (GSH, a biomarker of protective oxidative injury) were also determined in all dissected tissues. Pretreatment with Hesperidin (in group III) alleviated lung morphological changes noticed in I/R group and the levels of MDA and MPO were significantly decreased whereas those of GSH were significantly increased. Immunohistochemical study revealed a significant decrease in the iNOS. Hesperidin also significantly alleviated the formation of pulmonary edema as evidenced by the decreased organ wet/dry weight ratios. Hesperidin exerts a protective effect against lung damage induced by intestinal I/R injury in rats by reducing oxidative stress.

Hesperidin protects against cyclophosphamide-induced hepatotoxicity by upregulation of PPARgamma and abrogation of oxidative stress and inflammation.[Pubmed:25079140]

Can J Physiol Pharmacol. 2014 Sep;92(9):717-24.

The most important reason for the non-approval and withdrawal of drugs by the Food and Drug Administration is hepatotoxicity. Therefore, this study was undertaken to evaluate the protective effects of Hesperidin against cyclophosphamide (CYP)-induced hepatotoxicity in Wistar rats. The rats received a single intraperitoneal dose of CYP of 200 mg/kg body mass, followed by treatment with Hesperidin, orally, at doses of 25 and 50 mg/kg for 11 consecutive days. CYP induced hepatic damage, as evidenced by the significantly elevated levels of serum pro-inflammatory cytokines, serum transaminases, liver lipid peroxidation, and nitric oxide. As a consequence, there was reduced glutathione content, and the activities of the antioxidant enzymes superoxide dismutase, catalase, and glutathione peroxidase, were markedly reduced. In addition, CYP administration induced a considerable downregulation of peroxisome proliferator activated receptor gamma (PPARgamma) and upregulation of nuclear factor-kappa B (NF-kappaB) and inducible nitric oxide synthase (iNOS) mRNA expression. Hesperidin, in a dose-dependent manner, rejuvenated the altered markers to an almost normal state. In conclusion, Hesperidin showed a potent protective effect against CYP-induced oxidative stress and inflammation leading to hepatotoxicity. The study suggests that Hesperidin exerts its protective effect against CYP-induced hepatotoxicity through upregulation of hepatic PPARgamma expression and abrogation of inflammation and oxidative stress.

Hesperidin (HP) is a bioflavonoid that plays a role in plant defense and is abundant in citrus species, such as grapefruit, lemon and orange.

Hesperidin,520-26-3,Hesperetin 7-rutinoside,Natural Products, buy Hesperidin , Hesperidin supplier , purchase Hesperidin , Hesperidin cost , Hesperidin manufacturer , order Hesperidin , high purity Hesperidin