sinigrin and Inflammation

Sinigrin (allyl-glucosinolate or 2-propenyl-glucosinolate) is a natural aliphatic glucosinolate present in plants of the Brassicaceae family, such as broccoli and brussels sprouts, and the seeds of Brassica nigra (mustard seeds) which contain high amounts of sinigrin. Since ancient times, mustard has been used by mankind for its culinary, as well as medicinal, properties. It has been systematically described and evaluated in the classical Ayurvedic texts. Studies conducted on the pharmacological activities of sinigrin have revealed anti-cancer, antibacterial, antifungal, antioxidant, anti-inflammatory, wound healing properties and biofumigation. This current review will bring concise information about the known therapeutic activities of sinigrin. However, the information on known biological activities is very limited and, hence, further studies still need to be conducted and its molecular mechanisms also need to be explored. This review on the therapeutic benefits of sinigrin can summarize current knowledge about this unique phytocompounds.

Topics: Anti-Inflammatory Agents; Antioxidants; Brassica; Glucosinolates; Humans; Inflammation; Seeds; Wound Healing

Mainly found in brussels sprouts, broccoli, and black mustard seeds, sinigrin (2-propenyl glucosinolate) has enjoyed some attention currently for its effects on health and disease prevention. The present research design is aimed at investigating the effects of sinigrin on inflammation, oxidative stress (OS) and memory. Randomly, six groups of male Wistar rats were categorized into the control and experimental groups. The experimental groups were treated with sinigrin (10 and 20 mg/kg, orally). The control positive group was given the pentylenetetrazole (PTZ) treatment and the control negative one was given normal saline. All groups were kindled by the sub-threshold dose (35 mg/kg, i.p.) of PTZ for 12 times in one month. When the kindling procedure was done, the seizure behaviors and the behavioral function were evaluated. For cognitive parameters, the shuttle box test was employed. When the experiment was terminated, the rats were euthanized and their blood serum as well as brain samples were isolated for respective measuring of OS and gene expression parameters. The treatment with sinigrin significantly delayed the appearance of the seizure symptoms in comparison to that of the PTZ group. It also significantly increased the memory parameters like retention latency and the total time having been spent in the light compartment in the epileptic rats. In addition, sinigrin increased the superoxide dismutase and catalase levels. Treatment with sinigrin suppressed the Il1b and Nlrp3 gene expression at hippocampal level. In sum, sinigrin prevents inflammation, OS and memory impairment against the PTZ-kindling epilepsy in rats.

Topics: Animals; Epilepsy; Glucosinolates; Inflammation; Male; NLR Family, Pyrin Domain-Containing 3 Protein; Pentylenetetrazole; Rats; Rats, Wistar; Seizures

Diabetes mellitus (DM) is a common metabolic disorder which arises due to the improper carbohydrate metabolism, decreased secretion/activity of insulin, and genetic abnormalities, which result in the increased blood glucose level generally known as hyperglycemia. Diabetes holds an increased global prevalence in each year and is responsible for increased morbidity and mortality rates. Hence, the current investigation focusses to assess the antidiabetic potential of sinigrin on diabetic animal model through the suppression of inflammation. Diabetes was initiated to the animals via administering streptozotocin (STZ) and supplemented with the sinigrin at 25- and 50-mg/kg dose via oral route. The diabetic rats demonstrated the elevated glucose, food and water intake, kidney and liver weights, and reduced bodyweight and depleted insulin status. The sinigrin treatment remarkably improved and modulated these changes in diabetic animals. Additionally, the sinigrin supplementation also modulated the changes in glucose-6-phosphatase; fructose 1,6-bisphosphatase; AST; ALT; creatinine; and inflammatory mediators in the STZ-provoked diabetic animals. The levels of hexokinase, protein, and antioxidants also improved by the sinigrin treatment. The histological investigations of pancreas also witnessed the therapeutic actions of sinigrin, which is supported by the findings of biochemical examinations. Therefore, it was clear that the sinigrin supplementation displayed remarkable antidiabetic effect on STZ-initiated diabetic animals via modulating inflammation and other biochemical changes, which recommends that sinigrin could be a talented candidate for diabetes management in the future.

Topics: Animals; Antioxidants; Blood Glucose; Creatinine; Diabetes Mellitus, Experimental; Fructose; Glucose; Glucose-6-Phosphatase; Glucosinolates; Hexokinase; Hypoglycemic Agents; Inflammation; Inflammation Mediators; Insulin; Liver; Oxidative Stress; Rats; Streptozocin

The present study investigated the function of sinigrin in angiotensin II (Ang II)‑induced renal damage. The results demonstrated that systolic blood pressure (SBP) and diastolic blood pressure (DBP) were increased in Ang II‑challenged rats, and sinigrin treatment inhibited their increase. The levels of blood urea nitrogen (BUN) and serum creatinine (SCR) were increased by Ang II in the rats, and these were reversed by sinigrin in a dose‑dependent manner. In addition, the Ang II‑induced elevation of urinary protein levels was inhibited by sinigrin treatment. Glomerular basement membrane thickness and ECM degradation markers, such as collagen I, collagen IV and fibronectin, were suppressed by sinigrin in the Ang II‑challenged rats. Moreover, the levels of inflammatory regulators, including tumor necrosis factor‑α (TNF‑α), interleukin‑6 (IL‑6) and monocyte chemoattractant protein‑1 (MCP‑1), were reduced following sinigrin treatment of the Ang II‑challenged rats and in Ang II‑exposed proximal tubule epithelial cells. Furthermore, the superoxide dismutase (SOD) and catalase (CAT) levels were downregulated, whereas the malondialdehyde (MDA) levels were upregulated by Ang II; these effects were reversed by sinigrin treatment

Topics: Angiotensin II; Animals; Cell Line; Chemokine CCL2; Creatinine; Gene Expression Regulation; Glucosinolates; Humans; Inflammation; Kidney; Kidney Diseases; Malondialdehyde; MAP Kinase Signaling System; NF-kappa B; Oxidative Stress; Rats, Inbred SHR; Rats, Sprague-Dawley; Superoxide Dismutase; Tumor Necrosis Factor-alpha

Sinigrin (2-propenyl glucosinolate) is found mainly in broccoli, brussels sprouts, and black mustard seeds. Recently, sinigrin has received attention for its role in disease prevention and health. This study investigated the effect of sinigrin on macrophage function, including the activity of Nod-like receptor protein 3 (NLRP3) inflammasome. In a concentration-dependent manner, sinigrin inhibited lipopolysaccharide (LPS)-induced nitric oxide (NO) production and the expression of COX-2 and prostaglandin E2 (PGE2) in RAW 264.7 cells. In addition, sinigrin significantly suppressed the production of tumor necrosis factor (TNF)-α and interleukin (IL)-6 via suppression of MAPK phosphorylation and nuclear factor-kappa B (NF-κB) activity. Treatment with sinigrin decreased IL-1β and IL-18 production and concurrently suppressed NLRP3, apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), and caspase-1 expression in LPS/ATP-stimulated cells, suggesting that the blocking of NLRP3 inflammasome activation prevented the production of both cytokines. Collectively, these results suggest that sinigrin has immunomodulatory effects by suppressing the production of inflammatory mediators, possibly by inhibiting the NF-κB/MAPK pathways or NLRP3 inflammasome activation. Our findings also provide evidence that the pharmacological modulation of sinigrin could have an anti-inflammatory effect.

Topics: Animals; Anti-Inflammatory Agents; Cell Proliferation; Cytokines; Extracellular Signal-Regulated MAP Kinases; Glucosinolates; Inflammasomes; Inflammation; Inflammation Mediators; Lipopolysaccharides; Macrophages; Mice; NF-kappa B; Nitric Oxide; NLR Family, Pyrin Domain-Containing 3 Protein; RAW 264.7 Cells; Signal Transduction