Project Materials

PRELIMINARY INVESTIGATION ON EFFECTS OF BURANTASHI EXTRACT ON LIVER ENZYMES OF AIBINO MALE AND FEMALE.

ABSTRACT

The purpose of this study was to examine how Burantashi extract affected the liver enzymes of albino male and female whistar rats. Mostly prevalent in the northern region of Nigeria, burantashi is a common condiment for suya, or grilled meat. Enzymes that are vital to the liver’s activity and regulation are known as liver enzymes. The inability of a man to consistently or frequently achieve or sustain a penile erection strong enough for sexual activity is known as erectile dysfunction (ED) (2nd) International consultation on sexual dysfunction. June 28–July 1, 2003, Paris. Research on the mechanism underlying penile erection has greatly accelerated since Burantashi’s discovery and introduction. In the past five years, numerous preclinical and clinical papers on the peripheral regulation of and mediators involved in human penile erection have been published. There is discussion of the most commonly recognised risk factors for ED. The safety and efficacy of Burantasni Stem as a phosphodiesterase-5-inhibitor (PDE-5) used to treat erectile dysfunctions are the main topics of the study, along with human data.

CHAPTER ONE

INTRODUCTION

1.1 ERECTION PHYSIOLOGY

Complex physiological processes involving the central and peripheral nerve systems, as well as the hormonal and circulatory systems, are integrated during penile erection. The capacity to create and maintain an erection, ejaculate, and experience an orgasm is significantly impacted by any anomaly involving these systems, whether caused by medication or illness.

Laumann and associates (1999). The neurological and vascular systems are involved in the physiological process of erection, which starts in the brain. The brain’s neurotransmitters are the substances that cause an erection. Any form of psychological or physical stimulation triggers nerve signals to the vascular system, which leads to a substantial increase in blood flow to the penis.

The corpora cavernous and erectile tissues get blood from two arteries in the penis, which enlarge and enlarge due to elevated blood pressure and flow. because in order to retain stiffness, blood must remain in the penis.

Tunicae, which are fibrous elastic sheaths that tighten and stop blood from exiting the penis during electron flow, encircle an erectile tissue. An electron is saved when the penile muscles contract to block blood flow and open outflow channels.

1.2 THE ROLE OF HORMONES IN ERECTION

Progesterone/Oestrogen: ( The clitoral erection is brought on by these female hormones. She may become extremely moist but be unable to erect her clitoral and G-spot if her body contains too much oestrogen or too little testosterone.

(Haimen and others, 2002). The glans clitoris retreats into the clitoral hood, rendering it inconspicuous, whereas oestrogen tends to enlarge the bread, labia minors (inner lips), and clitoral hood.

Additionally, it thickens the vaginal lining, which prevents access to the G-spot. The clitoral and G-spot erections work by the same mechanism as the penis.

Acetylcholine, a neurotransmitter, operates through the parasympathetic sexual nerve to drive it. nitric oxide and cGMP, an erection dilator that burns testosterone continually without experiencing a burst or burning.

She is unable to pull off the G-spot and Clitoris glans. She may have low progesterone and an excess of oestrogens in her body if she is on birth control tablets.

An overloaded liver is unable to produce enough essential enzymes to synthesise enough NO, cGMP, and testosterone to support the clitoral and G-spot erection.

In fact, an excess of progesterone or oestrogen in the body will likely increase the size of the breasts while decreasing the penis, clitoral, and G-spot.

Testosterone: The hormone that the testicles produce, testosterone is

in charge of ensuring that male sexual characters are developed appropriately. While the band keeps the erection going, the pump helps the penis get erect. The generation of NO is correlated with testosterone levels in the blood.

Treatment with testosterone can lower insulin resistance and central obesity, which may help explain its positive effects on vascular NO and ED. In response to PDE-5 inhibitors, restoring erectile function and improving ED are two benefits of raising low testosterone levels.

1.3 PDE-5 Inhibition Mechanism of Action in Erection Dysfunction.

Penile erection is caused by smooth muscle relaxation mediated by the L-arginine nitric oxide guanglyl cyclase-cyclic guanosine monophosphate (cGMP) pathway and a spinal reflex. Nitric oxide is directly released by nerves and endothelial cells in the penis, where it reduces intracellular calcium levels and activates guanylyl cyclase to create cGMP. This causes trabecular and arterial smooth muscle to relax, which results in erection, venous constriction, and arterial dilatation.

The most common phosphodiesterase in the corpus cavernosum is phosphodiesterases (PDEs). By preventing its breakdown at the catalytic site, PDE-5 inhibitors like sildenafil enhance the endogenous rise in cGMP.

Normally, the catalytic site of PDE-5 breaks down cGMP. PDE-5’s enzymatic activity and the affinity of its allosteric (noncatalytic/GAF domains) sites for cGMP are both increased with phosphorylation. Enzymatic activity is further stimulated when cGMP binds to the allosteric site.

Therefore, negative feedback control of the cGMP pathway is mediated by PDE-5 phosphorylation and cGMP binding to the non-catalytic site.