mohammad khaksari hadad

The levels of IL-13, IL-4, IL-1B, TNF-α and IL-10 alter in the colon of people with ulcerative colitis. previous studies, it was found that shilajit (asphaltum) was effective in the improvement of ulcerative colitis.we guessed that the shilajit has been able to improve the ulcerative colitis by affecting the amount of cytokines.

The aim of the present study was to investigate the effects of shilajit on IL-13, IL-4, IL-1B, TNF-α and IL-10 in ulcerative colitis.

In this experimental study, 49 white male rats were randomly divided into 7 groups including sham groups, ulcerative colitis, Gavage vehicle, Gavage shilajit, sulfasalazine, Intra Anal Vehicle, Intra Anal shilajit. To produce ulcerative colitis 2 cc acetic acid (4%) was prescribed intra-rectal. 4 days after the induction of colitis, it was given 4 days: shilajit 250 mg / kg was used as a gavage or intra anal. Sulfasalazine was dosed at 250 mg / kg in the form of gavage.

The Gavage shilajit group increased IL-10, IL-4and decreased IL-1β, TNF-α compared to Gavage vehicle group. Shilajit has been able to close the levels of IL-4, IL-13, IL-10, TNF-α to normal values of the sham group.

Considering that the weight ratio of intestinal rat to the body of rat in the shilajit groups was lower than that of the sulfasalazine group, it can be shown that shilajit has been able to more reduce inflammation by making a more suitable change in cytokines in comparison with sulfasalazine.

Background and Cytokines regulate a broad range of biological and pathological processes. They play an important role in liver damage. Inflammatory and antioxidant factors are important causes of liver damage. Shilajit is known as an anti-inflammatory and antioxidant agent. Therefore, the main aim of this study was to determine the effect of Shilajit on levels of proinflammatory and anti-inflammatory cytokines in liver injury.
In this experimental study, 80 male Wistar rats were randomly divided into two main groups: A and B. Each group was organized into five subgroups: control, acetaminophen (A) or bile duct obstruction (BDL) (B), low dose, high dose, and vehicle. All subgroups except the controls in group A received 500 mg/ kg acetaminophen via IP injection, while BDL was performed in all subgroups in group B. Then in group A, two hours and in group B seven days after injury, the treatment subgroups with drug and vehicle received 150 mg/kg (low dose) and 250 mg/kg (high dose)shilajit and distilled water as vehicle, for one and six days, respectively. After completing treatment, liver samples were taken for laboratory analysis.
Low-dose Shilajit treatment reduced IL-10, IL-6, IL-1β, and TNF- α levels, which had been increased by a single dose of 500 mg/kg acetaminophen (p Shilajit is effective in reducing inflammation and liver damage caused by high-dose consumption of acetaminophen.

Objective(s)Gastric ulceration is induced by various forms of stress like surgery, ischemia and trauma. The female sex has more resistance to stress and the gastrointestinal lesions happen fewer than male sex. The purpose of this study was to evaluate the role of estradiol and progesterone on the gastric acid and pepsin levels following traumatic brain injury (TBI) induction.Materials and MethodsDiffuse TBI was induced by Marmarou method in female rats. Rats randomly assigned into 9 groups: intact, OVX (ovarectomized rat), Sham+OVX, TBI (intact rats under TBI), TBI+OVX (ovarectomized rats under TBI) and treated OVX rats with vehicle (sesame oil), E2 (estradiol), P4 (progesterone) or E2+P4 combination. The acid content and pepsin levels of each gastric washout sample were measured 5 days after the TBI induction.ResultsThere was no significant difference in gastric acid output between groups either after TBI induction or after treatment with E2 or P4 or E2+P4. Gastric pepsin levels were increased in Sham+OVX, TBI (P< 0.001) and TBI+OVX (P< 0.05) compared to intact group. Gastric pepsin levels were significantly lower in E2 and E2+ P4 treated rats than vehicle treated group (P< 0.01). P4 treatment increased gastric pepsin level compared to TBI+OVX group (P< 0.05) and this increment was higher than rats that were treated with the E2 and E2+P4 (P< 0.01).ConclusionThese results suggest that protective effect of estradiol and E2+P4 combination against mucosal damage after TBI, might be mediated by inhibition of pepsin secretion.

Following a traumatic brain injury (TBI), the excessive release of proinflammatory cytokines is major cause of cerebral edema that can cause permanent neuronal loss. This study examined the changes in brain concentrations of proinflammatory cytokines IL-1, IL-6, TNF-α and TGF- after different doses of estrogen or progesterone treatment in brain-injured rats at 6 and 24 h post-injury. Adult female rats were divided into 14 groups, and underwent either bilateral ovariectomy (12 groups) or sham surgery (2 groups). The hormones or vehicle were given intraperitoneally 0.5 h after TBI. Moderate TBI was induced by Marmarou method in TBI or treatment groups and brain levels of proinflammatory cytokines were measured 6 and 24 h post-injury. The results indicated that high dose of estrogen (E2) and low dose of progesterone (P1) increase brain levels of IL-1 6 h post-injury by 52.8% and 79.2%, respectively compared to the vehicle. By the 24th h post-injury brain IL-1 level was reduced 27.5% and 27%, respectively compared to vehicle, when estrogen low dose (E1) and E2 were administered. Progesterone high dose treatment reduced brain level of IL-6 by 45.9% at 6 h post-injury and P1 treatment reduced IL-6 level by 20.5% at 24 h post-injury when compared to the vehicle. The brain TNF-α level was reduced by 72.5% by P2 at 6 h and 48.5% by E2 at 24 h post-injury, when compared to the vehicle. In addition, TGF- level seem to be increased by E1 up to 3.37 times at 24 h post-injury compared to the vehicle. Both doses of hormones showed increased levels of TGF- at 6 h post-injury, when compared to the vehicle. We conclude that progesterone and estrogen may change the levels of proinflammatory cytokines in the acute or delayed phases after TBI and this may be one of the mechanisms by which hormones reduce cerebral edema.